FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Stroe, A Amin, F Kahn, T Knott, P AF Stroe, A Amin, F Kahn, T Knott, P TI Is circadian variation of plasma HVA related to its renal excretion? SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 BAYLOR COLL MED,HOUSTON VAMC,HOUSTON,TX 77030. MT SINAI SCH MED,BRONX VAMC,NEW YORK,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 457 EP 457 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300442 ER PT J AU Amin, F Kahn, T Knott, P AF Amin, F Kahn, T Knott, P TI Control of renal factors in plasma HVA measurements SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 BAYLOR COLL MED,HOUSTON VAMC,HOUSTON,TX 77030. MT SINAI SCH MED,BRONX VAMC,NEW YORK,NY. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 458 EP 458 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300443 ER PT J AU Moore, CM Christensen, JD Lafer, B Fava, M Renshaw, PF AF Moore, CM Christensen, JD Lafer, B Fava, M Renshaw, PF TI Phosphorous-31 magnetic resonance spectroscopy of the basal ganglia in depressed subjects SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 MCLEAN HOSP,BRAIN IMAGING CTR,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02144. HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA. RI Lafer, Beny/C-1055-2012; Lafer, Beny/F-9390-2015 OI Lafer, Beny/0000-0002-6132-9999; Lafer, Beny/0000-0002-6132-9999 NR 0 TC 0 Z9 0 U1 1 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 464 EP 464 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300449 ER PT J AU Adler, LE Waldo, MC McRae, KA Cawthra, E Nagamoto, HT Hoffer, L Johnson, M Gerhardt, G AF Adler, LE Waldo, MC McRae, KA Cawthra, E Nagamoto, HT Hoffer, L Johnson, M Gerhardt, G TI Differing relationship of cholinergic and catecholaminergic neurotransmission to sensory gating in schizophrenic patients, bipolar patients, and normal subjects SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 UNIV COLORADO,HLTH SCI CTR,DEPT PSYCHIAT,BOULDER,CO 80309. UNIV COLORADO,HLTH SCI CTR,DEPT PHARMACOL,BOULDER,CO 80309. DENVER VAMC,DENVER,CO. MED UNIV S CAROLINA SCH,INST PSYCHIAT,CHARLESTON,IL. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 514 EP 514 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300499 ER PT J AU Peskind, ER Elrod, R Digiacomo, L Veith, RC Raskind, MA AF Peskind, ER Elrod, R Digiacomo, L Veith, RC Raskind, MA TI CSF epinephrine in aging and Alzheimer's disease SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 VA PUGET SOUND HLTH CARE SYST,SEATTLE,WA 98108. UNIV WASHINGTON,SCH MED,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 1 PY 1996 VL 39 IS 7 BP 542 EP 542 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UE893 UT WOS:A1996UE89300527 ER PT J AU RemoldODonnell, E Rosen, FS Kenney, DM AF RemoldODonnell, E Rosen, FS Kenney, DM TI Defects in Wiskott-Aldrich syndrome blood cells SO BLOOD LA English DT Review ID X-LINKED THROMBOCYTOPENIA; BONE-MARROW TRANSPLANTATION; CARRIER DETECTION; CHROMOSOME INACTIVATION; PLATELET CALPAIN; B-CELLS; LYMPHOCYTES; MEMBRANE; PROTEIN; CD43 C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP RemoldODonnell, E (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI31541] NR 119 TC 98 Z9 98 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1996 VL 87 IS 7 BP 2621 EP 2631 PG 11 WC Hematology SC Hematology GA UC776 UT WOS:A1996UC77600002 PM 8639877 ER PT J AU Falzarano, G Krenger, W Snyder, KM Delmonte, J Karandikar, M Ferrara, JLM AF Falzarano, G Krenger, W Snyder, KM Delmonte, J Karandikar, M Ferrara, JLM TI Suppression of B-cell proliferation to lipopolysaccharide is mediated through induction of the nitric oxide pathway by tumor necrosis factor-alpha in mice with acute graft-versus-host disease SO BLOOD LA English DT Article ID BONE-MARROW TRANSPLANTATION; IFN-GAMMA; MONOCLONAL-ANTIBODY; L-ARGININE; T-CELLS; PERITONEAL-MACROPHAGES; SYNTHESIZING PATHWAY; EFFECTOR MECHANISM; INTERFERON-GAMMA; MESSENGER-RNA AB Graft-versus-host disease (GVHD) is associated with impaired B-cell responses. We investigated the mechanism of impaired proliferation of B cells in response to the mitogen lipopolysaccharide (LPS) by analyzing the production of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO), both of which have independently been described as important effector mechanisms in the pathogenesis of acute GVHD. A threefold decrease of mature surface Ig-positive (sIg(+)) B cells was observed in GVHD spleens isolated 2 weeks after transplant. However, proliferation of these cells in response to LPS was suppressed by more than 35-fold. Activated GVHD splenocytes secreted large amounts of TNF-alpha and NO in culture, Neutralization of TNF-alpha with anti-TNF-alpha antibody (Ab) both abrogated NO production and restored LPS-induced proliferation of B cells to levels found in non-GVHD control mice. The specific inhibition of NO synthesis with L(G)-monomethyl-arginine (NNMA) restored splenocyte responses but did not significantly reduce TNF-alpha levels, showing that TNF-alpha per se did not cause immunosuppression. These data show that, during GVHD, induction of the MO pathway is an important mechanism that mediates B-cell hyporesponsiveness to LPS and that this pathway is induced by TNF-alpha. (C) 1996 by The American Society of Hematology. C1 DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X FU NCI NIH HHS [CA 39542]; NIAID NIH HHS [AI 30018] NR 62 TC 35 Z9 35 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1996 VL 87 IS 7 BP 2853 EP 2860 PG 8 WC Hematology SC Hematology GA UC776 UT WOS:A1996UC77600029 PM 8639904 ER PT J AU DunussiJoannopoulos, K Weinstein, HJ Nickerson, PW Strom, TB Burakoff, SJ Croop, JM Arceci, RJ AF DunussiJoannopoulos, K Weinstein, HJ Nickerson, PW Strom, TB Burakoff, SJ Croop, JM Arceci, RJ TI Irradiated B7-1 transduced primary acute myelogenous leukemia (AML) cells can be used as therapeutic vaccines in murine AML SO BLOOD LA English DT Article ID T-CELLS; TUMOR REJECTION; CLONAL ANERGY; LYMPHOCYTES-T; GENE-TRANSFER; ANTIGEN; COSTIMULATION; EXPRESSION; MOLECULES; CD28 AB Recent studies have shown that tumor cells genetically modified by transduction of B7-1, a natural ligand for the T-cell costimulatory molecules CD28 and CTLA-4, are rejected in syngeneic hosts. In these reports, transformed cell lines and drug-selected cells have been used for vaccinations. To determine the effectiveness of B7-1-transduced primary acute myelogenous leukemia (AML) cells on the induction of antitumor immunity, we have studied a murine AML model in which primary AML cells were retrovirally transduced with the murine B7-1 cDNA. A defective retroviral producer clone expressing B7-1 and secreting a high titer of virus was used for infection of AML cells. Unselected transduced AML cells, expressing a high level of B7-1, were used for in vivo vaccinations. Our results show that one intravenous (IV) injection of irradiated B7-1-positive (B7-1(+)) AML cells can provide long-lasting (5 to 6 months) systemic immunity against subsequent challenge with wild-type AML cells. Furthermore, one exposure to irradiated B7-1(+) AML cells results in rejection of leukemia by leukemic mice when the vaccination occurs in the early stages of the disease. The antileukemia immunity is CD8(+) T-cell-dependent and B7/CD28-mediated, since in vivo treatment of mice with anti-CD8 monoclonal antibody or CTLA-4 Ig leads to abrogation of the specific antileukemia immune response. These results emphasize that B7-1 vaccines may have therapeutic usefulness for patients with AML. (C) 1996 by The American Society of Hematology. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,BOSTON,MA. CHILDRENS HOSP,MED CTR,DIV HEMATOL ONCOL,CINCINNATI,OH 45229. RP DunussiJoannopoulos, K (reprint author), DANA FARBER CANC INST,DEPT PEDIAT,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. OI Nickerson, Peter/0000-0002-7393-7799 NR 50 TC 89 Z9 89 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1996 VL 87 IS 7 BP 2938 EP 2946 PG 9 WC Hematology SC Hematology GA UC776 UT WOS:A1996UC77600039 PM 8639914 ER PT J AU Molrine, DC Guinan, EC Antin, JH Parsons, SK Weinstein, HJ Wheeler, C McGarigle, C Blanding, P Phillips, NR Kinsella, K Deans, K Ciamarra, A Goorin, A George, S Ambrosino, DM AF Molrine, DC Guinan, EC Antin, JH Parsons, SK Weinstein, HJ Wheeler, C McGarigle, C Blanding, P Phillips, NR Kinsella, K Deans, K Ciamarra, A Goorin, A George, S Ambrosino, DM TI Donor immunization with Haemophilus influenzae type b (HIB)-conjugate vaccine in allogeneic bone marrow transplantation SO BLOOD LA English DT Article ID VERSUS-HOST DISEASE; CAPSULAR POLYSACCHARIDE; CONJUGATE VACCINE; CHRONIC GRAFT; T-CELL; ANTIBODY; RECIPIENTS; OLIGOSACCHARIDE; INFECTIONS; IMMUNOGENICITY AB Bone marrow transplant patients are at increased risk for infections with polysaccharide encapsulated organisms and respond poorly to polysaccharide vaccines. We evaluated the effect of donor immunization with Haemophilus influenzae type b (HIB) polysaccharide-conjugate vaccine on recipient antibody responses following allogeneic bone marrow transplantation. Thirty-two allogeneic transplant patients and their donors were immunized before transplantation with HIB-conjugate, tetanus toroid and 23-valent pneumococcal vaccines. Following transplantation, patients received HIB-conjugate and tetanus toroid vaccines at 3, 6, 12, and 24 months and 23-valent pneumococcal vaccine at 12 and 24 months. Thirty-three patients with unimmunized donors were immunized following transplantation in an identical manner. Patients whose donors were immunized had significantly higher total anti-HIB antibody concentrations at 3 months (P = .0001), 6 months (P = .0001), 12 months (P = .0001), and 24 months (P = .002) after transplant compared with patients whose donors were unimmunized. Higher antitetanus toroid antibody concentrations were also noted in patients with immunized donors, whereas donor immunization with pneumococcal vaccine had no effect on antibody concentrations following transplantation. Donor immunization with HIB-conjugate vaccine resulted in higher antibody concentrations in patients as early as 3 months after allogeneic transplantation and may be an effective strategy to prevent HIB infections. (C) 1996 by The American Society of Hematology. C1 BRIGHAM & WOMENS HOSP,DIV HEMATOL & ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. RP Molrine, DC (reprint author), DANA FARBER CANC INST,INFECT DIS LAB,DEPT PHARM,DIV PEDIAT ONCOL,44 BINNEY ST,JFB ROOM 424,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA01730]; PHS HHS [A129623] NR 31 TC 50 Z9 51 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1996 VL 87 IS 7 BP 3012 EP 3018 PG 7 WC Hematology SC Hematology GA UC776 UT WOS:A1996UC77600049 PM 8639924 ER PT J AU Samiy, N Walton, DS Dreyer, EB AF Samiy, N Walton, DS Dreyer, EB TI Inhaled steroids: Effect on intraocular pressure in patients without glaucoma SO CANADIAN JOURNAL OF OPHTHALMOLOGY-JOURNAL CANADIEN D OPHTALMOLOGIE LA English DT Article DE steroid; inhaled; asthma; glaucoma; intraocular pressure ID ASTHMA AB Objective: To evaluate the risk of intraocular pressure (IOP) elevation in patients receiving inhaled steroid therapy. Design: Prospective study. Setting: Four private practices in New Jersey. Patients: A total of 187 patients (99 men and 88 women) with no documented history of glaucoma about to begin inhaled steroid therapy for various pulmonary conditions were enrolled, Of the 187, 183 were followed at 12 weeks. Interventions: Measurement of the IOP with the Tone-Pen before therapy was started and 12 weeks after therapy was started. Outcome measure: IOP. Results: No significant rise in IOP was observed. No patient had a rise in IOP greater than 4 mm Hg. Conclusions: Although isolated case reports indicate a definite risk of glaucoma in the presence of inhaled steroid therapy, the risk appears to be small. C1 MASSACHUSETTS EYE & EAR INFIRM,GLAUCOMA CONSULTAT SERV,BOSTON,MA 02114. FU NEI NIH HHS [R01-EY 10009] NR 8 TC 13 Z9 13 U1 0 U2 0 PU CANADIAN OPHTHAL SOC PI OTTAWA PA 1525 CARLING AVE SUITE 610, OTTAWA ON K1Z 8R9, CANADA SN 0008-4182 J9 CAN J OPHTHALMOL JI Can. J. Opthalmol.-J. Can. Opthalmol. PD APR PY 1996 VL 31 IS 3 BP 120 EP 123 PG 4 WC Ophthalmology SC Ophthalmology GA UJ729 UT WOS:A1996UJ72900005 PM 8743219 ER PT J AU Teicher, BA Holden, SA Ara, G Chen, G AF Teicher, BA Holden, SA Ara, G Chen, G TI Transforming growth factor-beta in in vivo resistance SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE transforming growth factor beta; drug resistance; in vivo resistance; cisplatin resistance; cyclophosphamide resistance ID TUMOR-CELL-LINES; ALKYLATING-AGENTS; RAT HEPATOCYTES; DNA-SYNTHESIS; TGF-BETA; LIVER; CIS-DIAMMINEDICHLOROPLATINUM(II); MECHANISM; INVITRO; INVIVO AB The potential role of transforming growth factor-beta in in vivo resistance was examined by administration of transforming growth factor-beta-neutralizing antibodies to animals bearing the EMT-6/Parent tumor or the antitumor alkylating resistant tumors, EMT-6/CTX or EMT-6/CDDP. Treatment of tumor-bearing animals with anti-TGF-beta antibodies by intraperitoneal injection daily on days 0-8 post-tumor cell implantation increased the sensitivity of the EMT-6/Parent tumor to cyclophosphamide (CTX) and cisplatin (CDDP) and markedly increased the sensitivity of the EMT-6/CTX tumor to CTX and the EMT-6/CDDP tumor to CDDP, as determined by tumor cell survival assay. Bone marrow granulocyte-macrophage colony-forming units (CFU-GM) survival was determined from these same animals. The increase in the sensitivity in the tumors upon treatment with the anti-TGF-beta antibodies was also observed in increased sensitivity of the bone marrow CFU-GM to CTX and CDDP. Treatment of non-tumor-bearing animals with the anti-TGF-beta regimen did not alter blood ATP or serum glucose level but did decrease serum lactate levels. This treatment also decreased hepatic glutathione, glutathione S-transferase, glutathione reductase, and glutathione peroxidase in non-tumor-bearing animals by 40-60% but increased hepatic cytochrome P450 reductase in these normal animals. Animals bearing the EMT-6/CTX and EMT-6/CDDP tumors had higher serum lactate levels than normal or EMT-6/Parent tumor-bearing animals; these were decreased by the anti-TGF-beta regimen. Treatment of animals bearing any of the three tumors with the anti-TGF-beta regimen decreased by 30-50% the activity of hepatic glutathione S-transferase and glutathione peroxidase, and increased by 35-80% the activity of hepatic cytochrome P450 reductase. In conclusion, treatment with transforming growth factor-beta-neutralizing antibodies restored drug sensitivity in the alkylating agent-resistant tumors, altering both the tumor and host metabolic states. C1 JOINT CTR RADIAT THERAPY, BOSTON, MA 02115 USA. RP Teicher, BA (reprint author), DANA FARBER CANC INST, 44 BINNEY ST, BOSTON, MA 02115 USA. FU NCI NIH HHS [R01 CA50174, P01 CA38493-09] NR 34 TC 29 Z9 32 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD APR PY 1996 VL 37 IS 6 BP 601 EP 609 DI 10.1007/s002800050435 PG 9 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA TZ390 UT WOS:A1996TZ39000015 PM 8612316 ER PT J AU Schenkman, M Riley, PO Pieper, C AF Schenkman, M Riley, PO Pieper, C TI Sit to stand from progressively lower seat heights - Alterations in angular velocity SO CLINICAL BIOMECHANICS LA English DT Article DE sit-to-stand; seat height; angular velocity; healthy individuals; chair rise; body position ID CHAIR HEIGHT; BIOMECHANICS; PERFORMANCE; MECHANICS; RISE; AGE AB This study investigates the influence of chair height on the dynamics of sit-to-stand for two age groups, Eleven young (25-36 years) and 10 older (61-79 years) adults participated. Subjects rose from chairs set at four heights relative to knee height, Motion was quantified using a bilateral active-marker-based motion analysis system. Subjects appeared to increase trunk flexion angular velocity to overcome mechanical difficulties of decreasing chair heights. This variable showed a main effect for chair height (P = 0.0001). Time at which knee, hip, and trunk extension angular velocity were attained each demonstrated a chair by age interaction effect (P < 0.05), Synchrony of body segment maximum extension angular velocities was altered for the older subjects at the lowest chair heights, suggesting that older individuals begin to change their performance as the task becomes more demanding. Relevance-Sitting to standing is one of the essential physical tasks used frequently throughout the day. Clinicians are frequently called upon to improve chair rise performance for those with functional limitations. Efforts are likely to be most successful if clinicians understand how healthy individuals accommodate to changing conditions (such as changing chair height) and use that information to interpret the performance of those with impairments and functional limitations. C1 DUKE UNIV,MED CTR,CTR STUDY AGING & HUMAN DEV,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT PHYS THERAPY,DURHAM,NC 27710. MASSACHUSETTS GEN HOSP,MGH BIOMOT LAB,BOSTON,MA 02114. RI Riley, Patrick/B-3053-2009 NR 13 TC 58 Z9 60 U1 0 U2 7 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0268-0033 J9 CLIN BIOMECH JI Clin. Biomech. PD APR PY 1996 VL 11 IS 3 BP 153 EP 158 DI 10.1016/0268-0033(95)00060-7 PG 6 WC Engineering, Biomedical; Orthopedics; Sport Sciences SC Engineering; Orthopedics; Sport Sciences GA UF359 UT WOS:A1996UF35900006 ER PT J AU Jacquot, S Modigliani, R Kuzniak, I Boumsell, L Bensussan, A AF Jacquot, S Modigliani, R Kuzniak, I Boumsell, L Bensussan, A TI Enhanced CD3 monoclonal antibody induced proliferation of colonic mucosal T lymphocytes in Crohn's disease patients free of corticosteroid or immunosuppressor treatment SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID INFLAMMATORY BOWEL-DISEASE; INTESTINAL LAMINA PROPRIA; NONHUMAN-PRIMATES; CELL SUBSET; ACTIVATION; ANTIGEN AB Mucosal lymphocytes are increasingly activated in Crohn's disease. In order to investigate this phenomenon we tested the response of cultured colonic mucosal T lymphocytes to CD3 activation. These lymphocytes were obtained by biopsy from control subjects and Crohn's disease patients. T cells from mucosa involved in Crohn's disease showed a higher CD3-induced proliferative response compared to control T lymphocytes (P < 0.01). T cells from uninvolved areas showed a wide range of response, ranging from normal to very high proliferative indices. Our results suggest that the exaggerated response of mucosal T lymphocytes, due to the impairment of the downregulation of the CD3-dependent signaling process, may contribute to the pathogenesis of Crohn's disease. (C) 1996 Academic Press Inc. RP Jacquot, S (reprint author), DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. RI Bensussan, Armand/E-5434-2017 NR 15 TC 3 Z9 3 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD APR PY 1996 VL 79 IS 1 BP 20 EP 24 DI 10.1006/clin.1996.0046 PG 5 WC Immunology; Pathology SC Immunology; Pathology GA UJ249 UT WOS:A1996UJ24900003 PM 8612347 ER PT J AU Better, N Janicek, MJ Annese, ML Kaplan, WD AF Better, N Janicek, MJ Annese, ML Kaplan, WD TI Mediastinal tumor presenting as a cardiac halo on equilibrium radionuclide angiography - A differential diagnosis to pericardial effusion SO CLINICAL NUCLEAR MEDICINE LA English DT Article C1 DANA FARBER CANC INST,DIV NUCL MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-9762 J9 CLIN NUCL MED JI Clin. Nucl. Med. PD APR PY 1996 VL 21 IS 4 BP 334 EP 335 DI 10.1097/00003072-199604000-00023 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA UE444 UT WOS:A1996UE44400023 PM 8925627 ER PT J AU Isler, MH Fogaca, MF Mankin, HJ AF Isler, MH Fogaca, MF Mankin, HJ TI Radiation induced malignant Schwannoma arising in a neurofibroma SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID NERVE SHEATH TUMORS; SARCOMAS; SURVIVAL AB Radiation induced sarcomas offer diagnostic and therapeutic challenges. The authors report an unusual case of radiation induced sarcoma arising 9 years after radiation therapy for chordoma, The location of this mass In the retroperitoneum and its intimate involvement with the spine raised difficult management issues, After limited resection was performed, consistent with the intraoperative diagnosis of a benign neurofibroma, foci of malignant transformation were found in areas of the specimen remote from the biopsy site, This complicated management of the sarcoma, The possibility of occult malignancy should be considered when evaluating tumors arising in a previously irradiated field, Thorough sampling at the time of biopsy is required to evaluate such lesions, particularly peripheral nerve sheath tumors. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED SURG,BOSTON,MA 02114. NR 20 TC 9 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD APR PY 1996 IS 325 BP 251 EP 255 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA UD415 UT WOS:A1996UD41500031 PM 8998885 ER PT J AU Schima, W Mukerjee, A Saini, S AF Schima, W Mukerjee, A Saini, S TI Contrast-enhanced MR imaging SO CLINICAL RADIOLOGY LA English DT Review ID POSTOPERATIVE LUMBAR SPINE; GADOPENTETATE DIMEGLUMINE; GD-DTPA; GADOLINIUM-DTPA; FAT-SUPPRESSION; MN-DPDP; CEREBRAL INFARCTION; UNENHANCED MR; IRON-OXIDE; CT C1 HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. RP Schima, W (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV ABDOMINAL IMAGING,32 FRUIT ST,BOSTON,MA 02114, USA. NR 108 TC 13 Z9 14 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9260 J9 CLIN RADIOL JI Clin. Radiol. PD APR PY 1996 VL 51 IS 4 BP 235 EP 244 DI 10.1016/S0009-9260(96)80339-4 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA UE988 UT WOS:A1996UE98800001 PM 8617034 ER PT J AU Johnson, MW Powelson, JA Auchincloss, H Delmonico, FL Cosimi, AB AF Johnson, MW Powelson, JA Auchincloss, H Delmonico, FL Cosimi, AB TI Selective use of veno-venous bypass in orthotopic liver transplantation SO CLINICAL TRANSPLANTATION LA English DT Article DE liver transplantation; veno-venous bypass; renal function ID HEPATIC TRANSPLANTATION; MANAGEMENT AB The use of veno-venous bypass (VVB) during the anhepatic phase of orthotopic liver transplantation (OLT) remains controversial. We employ VVB on a selective basis: patients who tolerate intra-operative supra-hepatic IVC test cross-clamping undergo OLT without VVB while patients who, despite maximal volume resuscitation, develop hemodynamic instability during test cross-clamping, undergo OLT with VVB. The records of 150 adult orthotopic liver allograft recipients transplanted at the Massachusetts General Hospital from January 1984 to December 1994 were reviewed to identify any potential adverse affects on peri-operative, 6 months, 1 year outcomes in recipients foregoing VVB during liver transplantation. Thirty-eight patients (25%) underwent OLT without VVB with actuarial survivals of 78.4% and 69% at 6 months and 1 year. 112 patients (75%) underwent OLT with VVB with actuarial survivals at 6 months and 1 year of 73% and 72%. Demographic data, UNOS status, and diagnoses were similar in each group. There were no significant differences in intra-operative PRBC requirements; lengths of hospital stay; retransplantation rates; or 30 day, 6 months and 1 year survivals between these two groups. There was no significant difference in renal function as determined by preoperative, peak post-operative, discharge serum creatinine levels, or number of patients requiring HD between these two groups. There were two major complications (1.8%) possibly resulting from VVB. In conclusion, patients who tolerate IVC test cross-clamping can safely undergo orthotopic liver transplantation without veno-venous bypass. In our experience, there were no significant differences in perioperative parameters, post-operative renal function, or short-term survival when compared to patients who, due to hemodynamic instability during IVC cross-clamping, underwent OLT with VVB. Given the potential complications associated with WE, we feel that in those patients who tolerate intra-operative IVC cross-clamping, it is better to proceed without the use of VVB. C1 MASSACHUSETTS GEN HOSP,GEN SURG SERV,TRANSPLANTAT UNIT,BOSTON,MA 02114. NR 12 TC 19 Z9 23 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0063 J9 CLIN TRANSPLANT JI Clin. Transplant. PD APR PY 1996 VL 10 IS 2 BP 181 EP 185 PG 5 WC Surgery; Transplantation SC Surgery; Transplantation GA UC922 UT WOS:A1996UC92200007 PM 8664515 ER PT J AU Streuli, M AF Streuli, M TI Protein tyrosine phosphatases in signaling SO CURRENT OPINION IN CELL BIOLOGY LA English DT Article ID SH2-CONTAINING PHOSPHOTYROSINE PHOSPHATASE; RECEPTOR-BETA; PHOSPHORYLATION; ACTIVATION; PP60(C-SRC); KINASES; SH-PTP2; BINDING AB During the past few years, molecular cloning has established the existence of a structurally diverse family of intracellular and transmembrane protein tyrosine phosphatases (PTPases). The importance of PTPases in signaling is best understood in three model systems: the mammalian transmembrane CD45 PTPase, the Drosophila Src homology (SH)2 domain containing corkscrew PTPase and its vertebrate homolog SH-PTP2, and the mouse SH2-domain-containing hematopoietic cell PTPase. Whereas CD45, corkscrew and SH-PTP2 positively regulate tyrosine phosphorylation, the hematopoietic cell PTPase negatively regulates or terminates signaling. Recent data indicate that several transmembrane PTPases mediate cell adhesion, suggesting that they effect adhesion-specific signaling events. RP Streuli, M (reprint author), DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA55547] NR 81 TC 157 Z9 159 U1 0 U2 2 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0955-0674 J9 CURR OPIN CELL BIOL JI Curr. Opin. Cell Biol. PD APR PY 1996 VL 8 IS 2 BP 182 EP 188 DI 10.1016/S0955-0674(96)80064-0 PG 7 WC Cell Biology SC Cell Biology GA UC439 UT WOS:A1996UC43900008 PM 8791415 ER PT J AU Oettinger, MA AF Oettinger, MA TI Cutting apart V(D)J recombination SO CURRENT OPINION IN GENETICS & DEVELOPMENT LA English DT Article ID STRAND BREAK REPAIR; BROKEN DNA-MOLECULES; PROTEIN-KINASE; SCID MUTATION; MOUSE THYMOCYTES; GENES; MICE; REARRANGEMENT; RAG-1; DEFICIENCY AB The past year has seen major advances in our understanding of the recombination mechanism by which antibody and T cell receptor genes are assembled during lymphoid development. The initial cleavage events can be carried out in vitro by purified RAG1 and RAG2 protein. In addition, a number of genes involved in later steps of the reaction have been cloned, opening the way for an in-depth biochemical analysis of this critical developmental process. RP Oettinger, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT BIOL MOLEC,WELLMAN 10,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [GM48026] NR 43 TC 18 Z9 18 U1 0 U2 1 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0959-437X J9 CURR OPIN GENET DEV JI Curr. Opin. Genet. Dev. PD APR PY 1996 VL 6 IS 2 BP 141 EP 145 DI 10.1016/S0959-437X(96)80042-6 PG 5 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA UE725 UT WOS:A1996UE72500002 PM 8722168 ER PT J AU Lynch, MW Rutecki, PA Sutula, TP AF Lynch, MW Rutecki, PA Sutula, TP TI The effects of seizures on the brain SO CURRENT OPINION IN NEUROLOGY LA English DT Article ID MEMORY; NMDA AB Since the time of Sommer's review of hippocampal pathology and Gower's tenet that 'seizures beget seizures' there has been interest in changes in brain structure and function that may be associated with epilepsy. From recent experimental studies and clinical observations, there is increasing evidence that epilepsy is not only associated with structural and functional alterations in the nervous system, but also that seizures induce a diverse variety of molecular, cellular, and functional alterations in the brain. C1 UNIV WISCONSIN,DEPT NEUROL,MADISON,WI 53792. UNIV WISCONSIN,DEPT NEUROSURG,MADISON,WI 53792. UNIV WISCONSIN,DEPT ANAT,MADISON,WI 53706. UNIV WISCONSIN,NEUROSCI TRAINING PROGRAM,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. FU NINDS NIH HHS [NS-28580, NS-25020] NR 70 TC 35 Z9 36 U1 0 U2 1 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 1350-7540 J9 CURR OPIN NEUROL JI Curr. Opin. Neurol. PD APR PY 1996 VL 9 IS 2 BP 97 EP 102 DI 10.1097/00019052-199604000-00007 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA UN971 UT WOS:A1996UN97100007 PM 8782975 ER PT J AU Giordano, M Castellino, P DeFronzo, RA AF Giordano, M Castellino, P DeFronzo, RA TI Differential responsiveness of protein synthesis and degradation to amino acid availability in humans SO DIABETES LA English DT Article ID WHOLE-BODY LEUCINE; LYSINE METABOLISM; YOUNG MEN; INSULIN; TURNOVER; GLUCOSE; PLASMA; MEAL; NUTRITION; KINETICS AB We investigated the effects of graded hyperaminoacidemia on protein metabolism in eight healthy, young (25 +/- 2 years), normal weight (BMI = 25 +/- 1 kg/m(2)) overnight-fasted human subjects. A balanced amino acid solution was infused for 180 min at five different rates: 0.5 (study I), 1.0 (study II), 2.0 (study III), 4.0 (study IV), and 6.0 (study V) mg . kg(-1). min(-1) on separate days in random order. Studies were performed with [1-C-14]leucine infusion and indirect calorimetry to calculate leucine oxidation (LOX), nonoxidative leucine disposal (NOLD) (an index of protein synthesis), and endogenous leucine flux (ELF) (an index of proteolysis). Basal total plasma amino acid concentrations averaged 1.85 +/- 0.1 mmol/l and increased to 2.27 +/- 0.1, 2.70 +/- 0.2, 3.84 +/- 0.2, 5.87 +/- 0.4, and 7.52 +/- 0.3 mmol/l in studies I-V, respectively. ELF decreased from a basal value of 2.27 +/- 0.2 to 2.12 +/- 0.2, 1.97 +/- 0.1, 1.73 +/- 0.2, 1.67 +/- 0.3, and 1.65 +/- 0.1 mu mol/l . kg(-1). min(-1) in studies I-V, respectively (P < 0.05 for study I vs. basal, P < 0.01 for studies II-V vs. basal, and NS for studies IV and V vs. study III). LOX increased from a basal value of 0.31 +/- 0.04 to 0.38 +/- 0.05, 0.41 +/- 0.02 0.64 +/- 0.04, 1.11 +/- 0.07, and 1.56 +/- 0.05 mu mol . kg(-1). min(-1) in studies I-V (all P < 0.01 vs. basal; P < 0.05-0.01 for each study vs. preceding study). Basal NOLD averaged 1.96 +/- 0.2 and did not change significantly in studies I and II (2.03 +/- 0.2 and 2.10 +/- 0.1 mu mol . kg(-1). min(-1)). In contrast, a significant increase in NOLD was observed in studies III, IV, and V (to 2.3 +/- 0.15, 2.74 +/- 0.2, and 3.25 +/- 0.7 mu mol . kg(-1). min(-1), respectively; all (P < 0.01 vs. basal; P < 0.05-0.01 for each study vs. preceding study). The net leucine balance (difference between ELF and NOLD) (-0.31 +/- 0.06 mu mol . kg(-1). min(-1)) became less negative in study I (P < 0.01 vs. basal) and positive during studies II-V when the rise in plasma total amino acid levels was greater than or equal to 50% above basal level (P < 0.01 vs. each preceding study). In conclusion, NOLD, ELF, and LOX exhibit a differential responsiveness to acute changes in substrate availability: 1) small increments (25-50%) in plasma amino acid levels inhibit ELF and stimulate LOX but have no effect on NOLD; 2) stimulation of NOLD is observed only with increments in plasma amino acid levels greater than or equal to 100% above basal values; and 3) increments in plasma amino acid concentrations >100% above basal values cause a progressive dose-related increase in LOX and NOLD but do not induce any further inhibition of ELF. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIABET DIV,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV NAPLES 2,INST INTERNAL MED & NEPHROL,NAPLES,ITALY. OI CASTELLINO, Pietro/0000-0002-9014-2007 NR 30 TC 55 Z9 55 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD APR PY 1996 VL 45 IS 4 BP 393 EP 399 DI 10.2337/diabetes.45.4.393 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UM981 UT WOS:A1996UM98100002 PM 8603758 ER PT J AU LopesVirella, MF Klein, RL Virella, G AF LopesVirella, MF Klein, RL Virella, G TI Modification of lipoproteins in diabetes SO DIABETES-METABOLISM REVIEWS LA English DT Review ID LOW-DENSITY-LIPOPROTEIN; MONOCYTE-DERIVED MACROPHAGES; HERITABLE HYPERLIPIDEMIC RABBIT; CIRCULATING IMMUNE-COMPLEXES; TUMOR NECROSIS FACTOR; SMOOTH-MUSCLE CELLS; SUBCUTANEOUS INSULIN INFUSION; NON-ENZYMATIC GLYCOSYLATION; HUMAN-ENDOTHELIAL-CELLS; CHOLESTERYL ESTER ACCUMULATION C1 RALPH H JOHSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC. FU NHLBI NIH HHS [HL46815] NR 180 TC 36 Z9 37 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0742-4221 J9 DIABETES METAB REV JI Diabetes-Metab. Rev. PD APR PY 1996 VL 12 IS 1 BP 69 EP 90 PG 22 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UJ863 UT WOS:A1996UJ86300006 PM 8861502 ER PT J AU Fuchs, PC Barry, AL Brown, SD Allen, S Doern, G Ferraro, MJ Hardy, D Hindler, J Jenkens, S McLaughlin, J Murray, P Sewell, D AF Fuchs, PC Barry, AL Brown, SD Allen, S Doern, G Ferraro, MJ Hardy, D Hindler, J Jenkens, S McLaughlin, J Murray, P Sewell, D TI Survey of antimicrobial activity of four commonly used third generation cephalosporins tested against recent bacterial isolates from ten American medical centers, and assessment of disk diffusion test performance SO DIAGNOSTIC MICROBIOLOGY AND INFECTIOUS DISEASE LA English DT Article ID TENTATIVE INTERPRETIVE STANDARDS; SPECTRUM BETA-LACTAMASES; SUSCEPTIBILITY TESTS; INCLUDING RECOMMENDATIONS; INVITRO ACTIVITY AB Over 2,000 clinical isolates from ten American medical centers were tested for susceptibility to cefotaxine, ceftriaxone, ceftizoxime, and ceftazidime by both broth microdilution and disk diffusion methods. Typically resistant (e.g. enterococci) and highly susceptible (e.g. streptococci) isolates showed no change in susceptibility patterns compared to previous surveys. Pseudomonas aeruginosa and Stenotrophomonas maltophilia exhibited significant decreases in susceptibility to these cephalosporins. Among Escherichia coli and Klebsiella spp isolates, two to three percent were resistant to one of the four drugs whereas they were very susceptible to the other three. Of the four antibiotics, the cefotaxime disk diffusion test results correlated best with the microdilution results. With the other three drugs the disk diffusion test yielded 1 to 9% more susceptible test results and 1 to 20% fewer resistant test results than broth microdilution when testing gram negative bacilli. The clinical significance of such discrepancies is not known, but the impact on antibiotic susceptibility surveys and antibiogram comparisons could be significant. C1 INDIANA UNIV,MED CTR,WORCESTER,MA. UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ST VINCENT HOSP,PORTLAND,OR. UNIV ROCHESTER,STRONG MEM HOSP,ROCHESTER,NY 14642. UNIV CALIF LOS ANGELES,MED CTR,LOS ANGELES,CA 90024. UNIV FLORIDA,MED CTR,JACKSONVILLE,FL 32209. UNIV NEW MEXICO,MED CTR,ALBUQUERQUE,NM 87131. BARNES HOSP,ST LOUIS,MO 63110. VET ADM MED CTR,PORTLAND,OR. RP Fuchs, PC (reprint author), INST CLIN MICROBIOL,POB 947,TUALATIN,OR 97062, USA. NR 12 TC 9 Z9 9 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0732-8893 J9 DIAGN MICR INFEC DIS JI Diagn. Microbiol. Infect. Dis. PD APR PY 1996 VL 24 IS 4 BP 213 EP 219 DI 10.1016/0732-8893(96)00028-4 PG 7 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA UV991 UT WOS:A1996UV99100007 PM 8831036 ER PT J AU Wen, ST Jackson, PK VanEtten, RA AF Wen, ST Jackson, PK VanEtten, RA TI The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene products SO EMBO JOURNAL LA English DT Article DE Abelson murine leukemia virus; p53; retino-blastoma protein; tyrosine kinase ID LARGE T-ANTIGEN; TYROSINE KINASE; CELL-CYCLE; PHILADELPHIA-CHROMOSOME; DIFFERENTIAL EXPRESSION; TRANSFORMING ABILITY; NUCLEOTIDE-SEQUENCE; ADENOVIRUS E1A; MESSENGER-RNA; COMMON SITES AB c-Abl is a non-receptor protein-tyrosine kinase lacking a clear physiological role. A clue to its normal function is suggested by overexpression of Abl in fibroblasts, which leads tea inhibition of cell growth, This effect requires tyrosine kinase activity and the Abl C-terminus. c-Abl is localized to the cell nucleus, where it can bind DNA, and interacts with the retinoblastoma protein, a potential mediator of the growth-inhibitory effect, Nuclear localization of Abl can be directed by a pentalysine nuclear localization signal in the Abl C-terminus. Here, we have identified two additional basic motifs im the Abl C-terminus, either of which can function independently of the pentalysine signal to localize Abl to the nucleus, Using a quantitative transfection assay, we show that both c-Abl and transforming Abl proteins inhibit entry into S phase and this effect is absolutely dependent on nuclear localization. Further, we demonstrate that the Abl cytostatic effect requires both the Rb and p53 tumor suppressor gene products. These results indicate that Abl inhibits cell proliferation by interacting with central elements of the cell cycle control apparatus in the nucleus, and suggest a direct connection between p53 and Rb in this growth-inhibitory pathway. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. NR 83 TC 163 Z9 165 U1 0 U2 4 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD APR 1 PY 1996 VL 15 IS 7 BP 1583 EP 1595 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UF658 UT WOS:A1996UF65800013 PM 8612582 ER PT J AU Albrecht, ED Aberdeen, GW Babischkin, JS Tilly, JL Pepe, GJ AF Albrecht, ED Aberdeen, GW Babischkin, JS Tilly, JL Pepe, GJ TI Biphasic developmental expression of adrenocorticotropin receptor messenger ribonucleic acid levels in the baboon fetal adrenal gland SO ENDOCRINOLOGY LA English DT Article ID 3-BETA-HYDROXYSTEROID DEHYDROGENASE ISOMERASE; LATE GESTATION; DEHYDROEPIANDROSTERONE FORMATION; STEROIDOGENIC ENZYMES; PITUITARY; ESTROGEN; CELLS; MIDGESTATION; METABOLISM; ACTIVATION AB We have previously shown an estrogen-dependent developmental regulation of placental oxidation of cortisol to cortisone that results in enhanced fetal pituitary ACTH production and the induction of steroidogenic enzymes in and de novo cortisol production by the fetal adrenal in the second half of baboon pregnancy. However, it is not known whether the receptor for ACTH is simultaneously generated at this time in development to provide a mechanism for mediating the tropic action of ACTH on steroidogenesis in the primate fetal adrenal gland. Therefore, in the present study we determined the levels of ACTH receptor messenger RNA (mRNA) and correlated ACTH receptor expression with appearance of the mRNA for Delta 5-3 beta-hydroxysteroid dehydrogenase/isomerase (3 beta HSD), the enzyme protein that signals functional maturation of the definitive cortical zone in the baboon fetal adrenal. A baboon ACTH receptor complementary DNA was cloned and hybridized with polyadenylated RNA isolated from baboon (Papio anubis) fetal adrenals obtained in early (days 58-64; RNA from seven baboon fetuses pooled to yield three samples), mid(days 99-103; RNA from five baboons pooled to yield four samples), and late (days 165-168; RNA of four individual baboon fetuses) gestation (term = 184 days). Expression of the primary 3.4-kilobase ACTH receptor mRNA transcript, determined by Northern blot and expressed as a ratio of beta-actin mRNA, was minimal early in gestation (mean +/- SE, 0.11 +/- 0.05 arbitrary densitometric units). However, fetal adrenal ACTH receptor mRNA levels increased (P < 0.001, by ANOVA) approximately 13-fold to 1.41 +/- 0.16 at midgestation, then declined by 70% (P < 0.001) to 0.41 +/- 0.10 in late gestation. To determine whether the decrease in ACTH receptor expression by the fetal adrenal in the second half of pregnancy reflected programmed cell death, the integrity of genomic DNA was assessed by P-32-labeled DNA gel electrophoresis and in situ DNA end labeling. Because DNA oligonucleosomes and apoptotic DNA strand breaks characteristic of apoptosis were absent in the adrenal glands of fetal baboons, the decline in ACTH receptor mRNA levels in the fetal adrenal did not seem to reflect programmed cell death. Expression of the single 2.0-kilobase mRNA transcript for 3 beta HSD, an enzyme localized specifically in the definitive zone of the fetal adrenal, was minimal in early (0.01 +/- 0.00 arbitrary units) and mid- (0.10 +/- 0.01) gestation. However, 3 beta HSD mRNA levels were markedly increased late in gestation to a value (1.38 +/- 0.34) approximately 13-fold greater (P < 0.001)than that in midgestation. These findings indicate that there was a biphasic monomodal developmental expression of the ACTH receptor in the baboon fetal adrenal, which contrasted with the progressive increase in adrenal weight, 3 beta HSD expression, and de novo cortisol production previously determined. Because the fetal adrenal is comprised mainly of the fetal cortical zone throughout gestation, the decrease in ACTH receptor expression between mid- and late gestation seems to occur primarily in the latter zone and may signal a selective decline in tropic responsivity of and Delta(5)-C-19-steroid, e.g. dehydroepiandrosterone, biosynthesis within the baboon fetal adrenal gland. C1 UNIV MARYLAND, SCH MED, CTR STUDIES REPROD, DEPT PHYSIOL, BALTIMORE, MD 21201 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED, DEPT OBSTET & GYNECOL,VINCENT CTR REPROD BIOL, BOSTON, MA 02114 USA. EASTERN VIRGINIA MED SCH, DEPT PHYSIOL, NORFOLK, VA 23501 USA. RP Albrecht, ED (reprint author), UNIV MARYLAND, SCH MED, FC BRESSLER RES LABS 11 019, DEPT OBSTET & GYNECOL, 655 W BALTIMORE ST, BALTIMORE, MD 21201 USA. FU NICHD NIH HHS [R01-HD-13294] NR 53 TC 21 Z9 22 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1996 VL 137 IS 4 BP 1292 EP 1298 DI 10.1210/en.137.4.1292 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UB891 UT WOS:A1996UB89100021 PM 8625902 ER PT J AU Loechner, KJ Kream, RM Dunlap, K AF Loechner, KJ Kream, RM Dunlap, K TI Calcium currents in a pituitary cell line (AtT-20): Differential roles in stimulus-secretion coupling SO ENDOCRINOLOGY LA English DT Article ID CORTICOTROPIN-RELEASING FACTOR; PRO-ACTH-ENDORPHIN; CA2+ CHANNELS; TUMOR-CELLS; ADRENOCORTICOTROPIN RELEASE; PERIPHERAL NEURONS; INHIBITION; DIVERSITY; SODIUM AB The purpose of the present investigation was to identify voltage-dependent calcium channel subtypes that control the release of ACTH in AtT-20 cells, a clonal mouse pituitary cell line. Using the perforated patch-clamp technique, we identified dihydropyridine (nimodipine)-, omega-Agatoxin IVA-, and omega-Conotoxin MVIIC-sensitive calcium currents. No omega-Conotoxin GVIA-sensitive currents are present in these cells. There also existed a considerable resistant component to the recorded inward current that was inhibited by cadmium, a nonselective calcium channel antagonist. Using RIA, we examined the contributions of each of the pharmacologically distinct calcium channel populations to CRH- or potassium chloride (KCl)-stimulated release of ACTH at various time intervals (10 sec to 60 min). We found that nimodipine markedly inhibited ACTH release at all intervals tested, whereas omega-Agatoxin TVA, omega-Conotoxin MVIIC, and omega-Conotoxin GVIA had no significant effect. Moreover, the inhibition by nimodipine was comparable to that seen after cadmium application, and the effects of these two antagonists were not additive. These data suggest that although AtT-20 cells possess dihydropyridine-, omega-Agatoxin IVA-, and omega-Conotoxin MVIIC-sensitive calcium channels as well as a considerable toxin-resistant current, only the dihydropyridine-sensitive calcium channels appear to be coupled to CRH- or KCl-induced ACTH release. C1 TUFTS UNIV, SCH MED, DEPT PHARMACOL & EXPTL THERAPEUT, BOSTON, MA 02111 USA. TUFTS UNIV NEW ENGLAND MED CTR, DEPT ANESTHESIOL, BOSTON, MA 02111 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, PEDIAT ENDOCRINE UNIT, BOSTON, MA 02114 USA. RP Loechner, KJ (reprint author), TUFTS UNIV, SCH MED, DEPT PHYSIOL, ROOM 709, 136 HARRISON AVE, BOSTON, MA 02111 USA. FU NINDS NIH HHS [NS-16483] NR 48 TC 20 Z9 20 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1996 VL 137 IS 4 BP 1429 EP 1437 DI 10.1210/en.137.4.1429 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UB891 UT WOS:A1996UB89100040 PM 8625921 ER PT J AU Noma, Y BonnerWeir, S Latimer, JB Davalli, AM Weir, GC AF Noma, Y BonnerWeir, S Latimer, JB Davalli, AM Weir, GC TI Translocation of glucokinase in pancreatic beta-cells during acute and chronic hyperglycemia SO ENDOCRINOLOGY LA English DT Article ID INDUCED INSULIN-SECRETION; GLUCOSE PHOSPHORYLATION; HEXOSE METABOLISM; HEXOKINASE; HETEROGENEITY; TRANSPORTER; RELEASE; ISLETS; LIVER; RAT AB Glucokinase (GK) plays a key role in the regulation of glucose-induced insulin secretion, and questions have been raised about its relationship to the glucose transporter GLUT2 and its function in diabetes. This study examined the location of immunostained GK and GLUT2 in beta-cells using confocal microscopy. On double stained sections from pancreases of normal fed rats, GLUT2 Texas Red staining was restricted to the plasma membrane, and GK fluorescein isothiocyanate staining was found in a limited area of cytoplasm that was perinuclear with slight extension toward the apical pole. The GK staining occupied 8.6 +/- 1.7% of total cytoplasmic area and was almost never adjacent to the GLUT2 staining of the plasma membrane. To determine whether the GK staining pattern is altered by metabolic perturbation, normal rats were made acutely hyperglycemic with iv glucose injections; after 20 min the GK staining changed from being localized to become diffusely distributed throughout the cytoplasm. To examine the influence of chronic hyperglycemia, rats were subjected to 90% partial pancreatectomy (Px), which produced glucose levels of 10.9-20.8 mM. When studied 6 or 14 days after Px, those rats with glucose levels greater than 17.7 mM had an altered GK staining pattern that was variable; in some beta-cells GK staining was diffuse and in others the localized staining pattern was preserved. GLUT2 staining was reduced overall, but variability between cells was observed, unlike the more uniform reductions seen with hyperglycemia of longer duration. Other rats received islet transplants to prevent hyperglycemia after Px; their GK and GLUT2 staining patterns were normal. These findings indicate that GK is translocated in association with acute and chronic hyperglycemia. The translocation of this key enzyme for glucose recognition by beta-cells may lead to altered rates of insulin secretion during acute perturbations of fuel provision and in the diabetic state. C1 DEACONESS HOSP, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02215 USA. JOSLIN DIABET CTR, DIV RES, BOSTON, MA 02215 USA. BRIGHAM & WOMENS HOSP, BOSTON, MA 02215 USA. FU NIDDK NIH HHS [DK-36836, DK-35449] NR 37 TC 42 Z9 43 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1996 VL 137 IS 4 BP 1485 EP 1491 DI 10.1210/en.137.4.1485 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UB891 UT WOS:A1996UB89100046 PM 8625927 ER PT J AU Schneyer, AL AF Schneyer, AL TI Measurement of activin in physiological fluids SO EUROPEAN JOURNAL OF ENDOCRINOLOGY LA English DT Editorial Material ID BOVINE FOLLICULAR-FLUID; INHIBIN ALPHA-SUBUNIT; HUMAN SERUM; MONOCLONAL-ANTIBODIES; BINDING-PROTEINS; MENSTRUAL-CYCLE; RADIOIMMUNOASSAY; OVARY RP Schneyer, AL (reprint author), MASSACHUSETTS GEN HOSP, NATL CTR INFERTIL RES, REPROD ENDOCRINE UNIT, BOSTON, MA 02114 USA. NR 23 TC 0 Z9 0 U1 0 U2 0 PU BIOSCIENTIFICA LTD PI BRISTOL PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT, ENGLAND SN 0804-4643 EI 1479-683X J9 EUR J ENDOCRINOL JI Eur. J. Endocrinol. PD APR PY 1996 VL 134 IS 4 BP 401 EP 402 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UJ668 UT WOS:A1996UJ66800004 PM 8640284 ER PT J AU Reiser, H Schneeberger, EE AF Reiser, H Schneeberger, EE TI Expression and function of B7-1 and B7-2 in hapten-induced contact sensitivity SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE contact sensitivity; B7-1; B7-2; hapten; CD80; CD86 ID T-CELL ACTIVATION; EPIDERMAL LANGERHANS CELLS; COUNTER-RECEPTOR; ANTIGEN; CTLA-4; INVIVO; PROLIFERATION; LYMPHOCYTES; MOLECULE; COMPLEX AB We analyzed the expression and function of the co-stimulatory molecules B7-1 (CD80) and B7-2 (CD86) during contact sensitivity reactions induced by the hapten 2,4-dinitrofluorobenzene (DNFB). In the normal skin, only a few epidermal Langerhans cells or dermal dendritic cells express B7-2. In contrast, following challenge with DNFB, expression of B7-2 is up-regulated in both epidermis and dermis. Importantly, B7-1 is induced later and at lower levels compared to B7-2. Intravenous injections of anti-B7-2 mAb, but not anti-B7-1 mAb partially inhibit the hapten-induced contact sensitivity reaction. Experiments in which mice are injected differentially with anti-B7-2 mAb, either before the afferent or before the efferent phase of the contact sensitivity response, suggest that B7-2 is important for successful antigen priming. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,ELECTRON MICROSCOPY UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP Reiser, H (reprint author), DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-36781]; NIAID NIH HHS [AI-33679, AI-35297] NR 38 TC 36 Z9 36 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD APR PY 1996 VL 26 IS 4 BP 880 EP 885 DI 10.1002/eji.1830260424 PG 6 WC Immunology SC Immunology GA UJ769 UT WOS:A1996UJ76900023 PM 8625983 ER PT J AU Kirch, SA Sudarsanam, P Oettinger, MA AF Kirch, SA Sudarsanam, P Oettinger, MA TI Regions of RAG1 protein critical for V(D)J recombination SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE V(D)J recombination; RAG1; RAG2; site-directed mutagenesis ID MUTATIONAL ANALYSIS; GENE; INVITRO; CELLS; HIV-1 AB The products of the recombination activating genes RAG1 and RAG2 are essential for activating V(D)J recombination, and thus are indispensable for the production of functional and diverse antigen receptors. To investigate the function of RAG1, we have tested a series of insertion and substitution mutations for their ability to induce V(D)J rearrangement on both deletional and inversional plasmid substrates. With these substrates we were also able to assess the effects of these mutations on both coding and signal joint formation, and to show that any one mutant affected all these reactions similarly. As defined previously, the core active regions of RAG1 and RAG2 permit the deletion of 40% and 25%, respectively, of well-conserved sequence. We show here that this ''dispensable'' region of RAG1 is not necessary for coding joint formation or for recombination of an integrated substrate, and that this portion is not functionally redundant with the ''dispensable'' region of RAG2. Recombination with these core regions is also still subject to the 12/23 joining rule. Further, the minimal essential core region of RAG1 can be located within an even smaller portion of the gene. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA. HARVARD UNIV,SCH MED,DEPT GENET,CAMBRIDGE,MA. FU NIGMS NIH HHS [R01GM48026] NR 29 TC 52 Z9 52 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD APR PY 1996 VL 26 IS 4 BP 886 EP 891 DI 10.1002/eji.1830260425 PG 6 WC Immunology SC Immunology GA UJ769 UT WOS:A1996UJ76900024 PM 8625984 ER PT J AU Uddin, S Yetter, A Katzav, S Hofmann, C White, MF Platanias, LC AF Uddin, S Yetter, A Katzav, S Hofmann, C White, MF Platanias, LC TI Insulin-like growth factor-1 induces rapid tyrosine phosphorylation of the vav proto-oncogene product SO EXPERIMENTAL HEMATOLOGY LA English DT Article DE insulin-like growth factor-1; tyrosine phosphorylation; vav proto-oncogene ID PROTOONCOGENE PRODUCT; HEMATOPOIETIC-CELLS; PHOSPHATIDYLINOSITOL 3'-KINASE; SIGNALING PATHWAYS; IRS-1; RECEPTOR; DOMAIN; MITOGENESIS; DEFINES; GRB2 AB The vav proto-oncogene product (p95(vav)) is specifically expressed in cells of hematopoietic origin and has one src homology 2 (SH2) domain, two SH3 domains, and motifs typical of guanine exchange factors. Insulin-like growth factor-1 (IGF-1) receptors are expressed on a variety of hematopoietic cells and, upon ligand binding, mediate signals regulating hematopoietic cell proliferation. We studied the phosphorylation status of p95(vav) in the U-266 human myeloma cell line, in response to IGF-1 stimulation. Immunoblotting experiments with an antiphosphotyrosine monoclonal antibody disclosed that p95(vav) is phosphorylated on tyrosine in an IGF-1-dependent manner. The tyrosine phosphorylation of p95(vav) was rapid, appearing within 5 minutes of IGF-1 treatment, and transient, diminishing by 90 minutes. Similar results were obtained when the mouse plasmacytoma J558L cell line was studied. IGF-1-dependent tyrosine phosphorylation of p95(vav) was also seen in the 32D mouse myeloid cell line that lacks expression of insulin receptor substrate (IRS) proteins, suggesting that it is not regulated by activation of the IRS-signaling system. Taken together, these data suggest that the vav proto-oncogene is a substrate for the IGF-1 receptor tyrosine kinase and may be involved in the signal transduction of IGF-1 in cells of hematopoietic origin. C1 LOYOLA UNIV,DEPT MED,DIV HEMATOL ONCOL,MAYWOOD,IL 60153. EDWARD HINES VET ADM MED CTR,RES SERV,HINES,IL 60141. EDWARD HINES VET ADM MED CTR,DEPT MED,HINES,IL 60141. MCGILL UNIV,JEWISH GEN HOSP,LADY DAVIS INST,MONTREAL,PQ H3T 1E2,CANADA. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-38712, DK-43808] NR 44 TC 14 Z9 14 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD APR PY 1996 VL 24 IS 5 BP 622 EP 627 PG 6 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA UE814 UT WOS:A1996UE81400006 PM 8605967 ER PT J AU Babyatsky, MW Rossiter, G Podolsky, DK AF Babyatsky, MW Rossiter, G Podolsky, DK TI Expression of transforming growth factors alpha and beta in colonic mucosa in inflammatory bowel disease SO GASTROENTEROLOGY LA English DT Article ID INTESTINAL EPITHELIAL-CELLS; FACTOR RECEPTOR; CANCER LINES; TGF-BETA; FACTOR-BETA-1; NEUTROPHILS AB Background & Aims: Transforming growth factors (TGFs) alpha and beta are key regulatory peptides that modulate mucosal cell populations critical to inflammatory bowel disease. The aim of this study was to assess TGF-alpha and TGF-beta expression in human colonic mucosa. Methods: TGF-alpha and TGF-beta expression was assessed in colonic mucosa from patients with ulcerative colitis, patients with Crohn's disease, and controls by Northern blot analysis, in situ hybridization, and bioassay. Results: TGF-alpha messenger RNA expression localized to the villous tips of the small intestine and the surface epithelium of the colon. TGF-alpha expression was enhanced 2.3-fold in inactive ulcerative colitis mucosa relative to active ulcerative colitis, Crohn's disease, or normal controls. Enhanced expression correlated with duration of disease. TGF-beta expression was increased in affected mucosa from both patients with ulcerative colitis and Crohn's disease with active disease. TGF-beta 1 messenger RNA expression in ulcerative colitis and Crohn's disease localized mostly to cells of the lamina propria with the highest concentration in inflammatory cells closest to the luminal surface. Conclusions: TGF-alpha may contribute to epithelial hyperproliferation and the increased risk of malignancy in long-standing ulcerative colitis. TGF-beta may be a key cytokine during periods of active inflammation, modulating epithelial cell restitution and functional features of cells within the lamina propria. C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. MT SINAI MED CTR, DIV GASTROINTESTINAL, NEW YORK, NY 10029 USA. FU NIDDK NIH HHS [DK43351, DK41557] NR 41 TC 258 Z9 265 U1 1 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 BP 975 EP 984 DI 10.1053/gast.1996.v110.pm8613031 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UD846 UT WOS:A1996UD84600001 PM 8613031 ER PT J AU Atiya, A Moldovan, S Adrian, T Coy, D Walsh, J Brunicardi, FC AF Atiya, A Moldovan, S Adrian, T Coy, D Walsh, J Brunicardi, FC TI Intraislet somatostatin inhibits insulin but not islet amyloid polypeptide secretion via a subtype-2 somatostatin receptor in the isolated perfused human pancreas. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT SURG, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, MED CTR, LOS ANGELES, CA 90024 USA. CREIGHTON UNIV, DEPT PHYSIOL, OMAHA, NE 68178 USA. TULANE UNIV, DEPT MED, NEW ORLEANS, LA 70118 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1373 EP A1373 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705464 ER PT J AU BelkindGerson, J Park, S Lewis, JD Kaplan, LM AF BelkindGerson, J Park, S Lewis, JD Kaplan, LM TI Several neurotrophins and ciliary neurotrophic factor are specifically expressed by rat and human intestinal epithelial cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, BOSTON, MA USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A791 EP A791 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703148 ER PT J AU Blumberg, R Story, C Wu, Z Christ, A Polischuk, J Israel, E Simister, N AF Blumberg, R Story, C Wu, Z Christ, A Polischuk, J Israel, E Simister, N TI Functional major histocompatibility complex (MHC) class I-related Fc receptor expression in human adult enterocytes and intestinal epithelial cell (IEC) lines. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, CAMBRIDGE, MA 02138 USA. BRANDEIS UNIV, WALTHAM, MA 02254 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A868 EP A868 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703453 ER PT J AU Carroll, N Choicca, EA Tanabe, KK AF Carroll, N Choicca, EA Tanabe, KK TI Gene transfer and cytoxicity mediated by recombinant herpes simplex virus vectors SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1377 EP A1377 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705480 ER PT J AU Chang, L Munakata, J An, K Saba, L Naliboff, B Procaccino, F Mayer, EA AF Chang, L Munakata, J An, K Saba, L Naliboff, B Procaccino, F Mayer, EA TI Evidence for the activation of endogenous pain modulation system in ulcerative colitis (UC). SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, HARBOR MED CTR, CTR INFLAMMATORY BOWEL DIS, TORRANCE, CA 90509 USA. UNIV CALIF LOS ANGELES, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT PHYSIOL & MED, CURE DIGEST DIS RES CTR, NEUROENTER BIOL GRP, LOS ANGELES, CA 90073 USA. NR 0 TC 8 Z9 8 U1 1 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A645 EP A645 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702564 ER PT J AU Chen, MC Bunnett, N Soll, AH AF Chen, MC Bunnett, N Soll, AH TI Endogenous ligands for the epidermal growth factor receptor (EGFR) regulate tight junction (TJ) permeability. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, W LOS ANGELES VET AFFAIRS MED CTR, DIGEST DIS RES CTR, LOS ANGELES, CA 90078 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A80 EP A80 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73700314 ER PT J AU Chung, DC Louis, DN GraemeCooke, F Warshaw, AL Arnold, A AF Chung, DC Louis, DN GraemeCooke, F Warshaw, AL Arnold, A TI Evidence for a novel pancreatic islet cell tumor suppressor gene with clinical prognostic implications SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, LAB ENDOCRINE ONCOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, LAB ENDOCRINE ONCOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT SURG, BOSTON, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A504 EP A504 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702002 ER PT J AU Chung, DC Louis, DN GraemeCooke, F Warshaw, AL Arnold, A AF Chung, DC Louis, DN GraemeCooke, F Warshaw, AL Arnold, A TI Analysis of the retinoblastoma gene in pancreatic islet cell tumors SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, LAB ENDOCRINE ONCOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A383 EP A383 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701524 ER PT J AU Chung, RT Kawashima, T Kaplan, LM AF Chung, RT Kawashima, T Kaplan, LM TI Expressed HCV NS5B possesses primer-dependent RNA polymerase activity. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1172 EP A1172 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704666 ER PT J AU Cohen, PA Mak, KM Kessova, I Koivisto, T Mishin, VM Rosman, AS Lieber, CS AF Cohen, PA Mak, KM Kessova, I Koivisto, T Mishin, VM Rosman, AS Lieber, CS TI Immunohistochemical determination of cytochrome P4502E1 in formalin-fixed, paraffin-embedded liver samples correlates with Western blot analysis. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR, CTR ALCOHOL RES & TREATMENT, NEW YORK, NY 10468 USA. MT SINAI SCH MED, NEW YORK, NY 10468 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1173 EP A1173 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704669 ER PT J AU Dohmen, K Baraona, E Ishibashi, H Pozzato, G Moretti, M Matsunaga, C Fujimoto, K Lieber, CS AF Dohmen, K Baraona, E Ishibashi, H Pozzato, G Moretti, M Matsunaga, C Fujimoto, K Lieber, CS TI Ethnic differences in gastric sigma-ADH activity and ethanol first-pass metabolism. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR, NEW YORK, NY USA. MT SINAI SCH MED, NEW YORK, NY USA. KYUSHU UNIV, DEPT INTERNAL MED 1, FUKUOKA 812, JAPAN. UNIV TRIESTE, INST CLIN MED, I-34127 TRIESTE, ITALY. SAGA MED SCH, GI DIV, SAGA, JAPAN. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1183 EP A1183 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704707 ER PT J AU Eskandari, S Marvizon, JC Ennes, HS Lembo, T Mayer, EA AF Eskandari, S Marvizon, JC Ennes, HS Lembo, T Mayer, EA TI Desensitization of calcium responses of cultured rat dorsal horn neurons to substance P. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED,CURE,DIGEST DIS RES CTR, NEUROENTER BIOL GRP, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT PHYSIOL,CURE,DIGEST DIS RES CTR, NEUROENTER BIOL GRP, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1070 EP A1070 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704259 ER PT J AU Fass, R Higa, L Kodner, A Naliboff, B Mayer, EA AF Fass, R Higa, L Kodner, A Naliboff, B Mayer, EA TI Chronic mucosal inflammation of the esophagus in gastroesophageal reflux disease (GERD) is not associated with mechanical hyperalgesia. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, DEPT MED, CURE, LOS ANGELES, CA 90024 USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A662 EP A662 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702631 ER PT J AU Fischer, C Bode, B Souba, W AF Fischer, C Bode, B Souba, W TI Differential and selective induction of amino acid transport activity in the tumor-influenced hepatocyte. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1385 EP A1385 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705511 ER PT J AU Foitzik, T Stufler, M Hotz, HG Klinnert, HJ Wagner, J Warshaw, AL Schulzke, JD Fromm, M Buhr, HJ AF Foitzik, T Stufler, M Hotz, HG Klinnert, HJ Wagner, J Warshaw, AL Schulzke, JD Fromm, M Buhr, HJ TI Glutamine stabilizes intestinal permeability and reduces pancreatic infection in acute experimental pancreatitis SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 FREE UNIV BERLIN, KLINIKUM BENJAMIN FRANKLIN, DEPT SURG, W-1000 BERLIN, GERMANY. FREE UNIV BERLIN, KLINIKUM BENJAMIN FRANKLIN, DEPT GASTROENTEROL, W-1000 BERLIN, GERMANY. FREE UNIV BERLIN, KLINIKUM BENJAMIN FRANKLIN, DEPT MICROBIOL, W-1000 BERLIN, GERMANY. FREE UNIV BERLIN, KLINIKUM BENJAMIN FRANKLIN, DEPT CLIN PHYSIOL, W-1000 BERLIN, GERMANY. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT SURG, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1385 EP A1385 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705512 ER PT J AU Foley, MK Inoue, Y Souba, WW Sarr, MG AF Foley, MK Inoue, Y Souba, WW Sarr, MG TI Extrinsic denervation downregulates transport of glutamine and other nutrients in jejunum SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MAYO CLIN & MAYO FDN, DEPT SURG, ROCHESTER, MN 55905 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A324 EP A324 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701291 ER PT J AU Forcione, DG Sands, B Rustgi, A Podolsky, DK Pillai, S AF Forcione, DG Sands, B Rustgi, A Podolsky, DK Pillai, S TI An increased risk of Crohn's disease in individuals who inherit the HLA class II DRB3*0301 allele. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, CTR CANC, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A908 EP A908 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703615 ER PT J AU Gerweck, KK Cheung, AM Wong, DKH AF Gerweck, KK Cheung, AM Wong, DKH TI Comparison of biochemical and virological responses to interferon therapy in chronic hepatitis C: A meta-analysis SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH PUBL HLTH, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1196 EP A1196 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704760 ER PT J AU Gilbert, RJ Daftary, S Campbell, T Weisskoff, RM AF Gilbert, RJ Daftary, S Campbell, T Weisskoff, RM TI Patterns of lingual deformation associated with the accommodation and propulsion phases of deglutition. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, NMR CTR, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT RADIOL, BOSTON, MA 02114 USA. ST ELIZABETHS MED CTR, DIV GASTROENTEROL, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A669 EP A669 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702661 ER PT J AU Gilbert, RJ Reese, TG Daftary, S Weisskoff, RM Wedeen, VJ AF Gilbert, RJ Reese, TG Daftary, S Weisskoff, RM Wedeen, VJ TI Characterization of lingual myoarchitecture by NMR imaging of water diffusion anisotropy. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, NMR CTR, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT RADIOL, BOSTON, MA 02114 USA. ST ELIZABETHS MED CTR, DIV GASTROENTEROL, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A669 EP A669 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702659 ER PT J AU Goke, MN Zuk, A Podolsky, DK AF Goke, MN Zuk, A Podolsky, DK TI Regulation and function of extracellular matrix in intestinal epithelial restitution SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A118 EP A118 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73700469 ER PT J AU Gralnek, IM Jensen, DM Jensen, ME Cheng, S Gornbein, J Kovacs, TOG Jutabha, R AF Gralnek, IM Jensen, DM Jensen, ME Cheng, S Gornbein, J Kovacs, TOG Jutabha, R TI Direct costs of hospital care in patients with active esophagogastric variceal hemorrhage treated with emergency endoscopic sclerotherapy or rubber band ligation in a prospective randomized trial. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1200 EP A1200 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704778 ER PT J AU Hanada, S Shioda, T Isselbacher, KJ Takahashi, H AF Hanada, S Shioda, T Isselbacher, KJ Takahashi, H TI Immunotherapy of human colon cancer by antibody-mediated induction of apoptosis SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MGH, CTR CANC, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A525 EP A525 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702089 ER PT J AU Higa, L Kodner, A Mayer, EA Fass, R AF Higa, L Kodner, A Mayer, EA Fass, R TI Stimulus and site specific induction of hiccups in the esophagus of normal subjects. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, DEPT MED, NEUROENTER BIOL GRP, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A678 EP A678 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702697 ER PT J AU Hocker, M Wu, HJ Nicholls, P OConnor, DT Wang, TC AF Hocker, M Wu, HJ Nicholls, P OConnor, DT Wang, TC TI The mouse chromogranin a promoter is regulated by gastrin through an upstream GC-rich sequence. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. UNIV CALIF SAN DIEGO, DEPT MED, SAN DIEGO, CA 92103 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1081 EP A1081 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704303 ER PT J AU Hocker, M Zhang, XS Wang, TC AF Hocker, M Zhang, XS Wang, TC TI Gastrin regulates the histidine decarboxylase promoter through an MAP kinase-dependent signaling pathway. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1080 EP A1080 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704302 ER PT J AU Hoppin, AG Jasper, MS Kaplan, LM AF Hoppin, AG Jasper, MS Kaplan, LM TI Elevated expression of the rat obese gene in subcutaneous fat of genetically obese and castrated rats. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A806 EP A806 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703207 ER PT J AU Inatomi, N Yakicier, MC Baba, S Isselbacher, KJ Takahashi, H AF Inatomi, N Yakicier, MC Baba, S Isselbacher, KJ Takahashi, H TI Expression of vascular endothelial growth factor genes in human primary and metastatic colon cancer SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. HAMAMATSU UNIV SCH MED, DEPT SURG, HAMAMATSU, SHIZUOKA 43131, JAPAN. MGH, CTR CANC, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A533 EP A533 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702119 ER PT J AU Israel, EJ Taylor, S Mizoguchi, E Bhan, A Simister, N AF Israel, EJ Taylor, S Mizoguchi, E Bhan, A Simister, N TI An MHC class I-related Fc-receptor is present in human intestinal epithelial cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, PROGRAM PEDIAT GASTROENTEROL, BOSTON, MA USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT NUTR & PATHOL, BOSTON, MA USA. BRANDEIS UNIV, DEPT BIOL, WALTHAM, MA 02254 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A931 EP A931 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703706 ER PT J AU Jenkins, TD Nakagawa, H Zukerberg, LR Wang, TC Rustgi, AK AF Jenkins, TD Nakagawa, H Zukerberg, LR Wang, TC Rustgi, AK TI Carcinogen induced murine model of esophageal cancer: Effect of N-nitrosomethylbenzylamine. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED, MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A536 EP A536 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702133 ER PT J AU Jenkins, TD Nakagawa, H Rustgi, AK AF Jenkins, TD Nakagawa, H Rustgi, AK TI PMA regulation of an Epstein-Barr Virus promoter in esophageal squamous epithelial cells SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, SCH MED, MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A536 EP A536 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702131 ER PT J AU Kanai, M Rosenberg, IM Podolsky, DK AF Kanai, M Rosenberg, IM Podolsky, DK TI Functional evidence for a novel ligand involved in FGFR3 mediated colonic epithelial cell proliferation. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1086 EP A1086 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704324 ER PT J AU Kaneko, H Rhue, N Nagai, N Mori, S Yamashita, K Yamaguchi, C Tache, Y Mitsuma, T AF Kaneko, H Rhue, N Nagai, N Mori, S Yamashita, K Yamaguchi, C Tache, Y Mitsuma, T TI Central distribution and action of adrenomedullin (AM) to induce gastric protection against ethanol in rats. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,CURE, DIGEST DIS RES CTR, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, BRAIN RES INST, LOS ANGELES, CA 90024 USA. AICHI MED UNIV, DEPT INTERNAL MED 4, NAGAKUTE, AICHI, JAPAN. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1087 EP A1087 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704327 ER PT J AU Kaneko, H Tanaka, S Kaunitz, JD Nagai, H Mitsuma, T Tache, Y AF Kaneko, H Tanaka, S Kaunitz, JD Nagai, H Mitsuma, T Tache, Y TI Central corticotropin-releasing factor (CRF)-induced gastric protection against ethanol through sympathetic-adrenergic pathways in rats. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,CURE, DIGEST DIS RES CTR, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, BRAIN RES INST, LOS ANGELES, CA 90024 USA. AICHI MED UNIV, DEPT INTERNAL MED 4, NAGAKUTE, AICHI, JAPAN. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1086 EP A1086 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704326 ER PT J AU Kaneko, H Nagai, H Mitsuma, T Tache, Y AF Kaneko, H Nagai, H Mitsuma, T Tache, Y TI Central corticotropin-releasing factor (CRF)-stimulated gastric bicarbonate secretion through pituitary and sympathetic pathways in rats. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, DIGEST DIS RES CTR, CURE, DEPT MED, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, BRAIN RES INST, LOS ANGELES, CA 90024 USA. AICHI MED UNIV, DEPT INTERNAL MED 4, AICHI, JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A148 EP A148 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73700588 ER PT J AU Koh, TJ Nicholls, PJ Wang, TC AF Koh, TJ Nicholls, PJ Wang, TC TI Glycine-extended gastrin promotes growth of a human hepatoma cell line. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1089 EP A1089 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704336 ER PT J AU Lembo, T Munakata, J Naliboff, B Saba, L Mayer, EA AF Lembo, T Munakata, J Naliboff, B Saba, L Mayer, EA TI Opioids differentially affect human perception of visceral and somatic pain. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, DEPT PHYSIOL & MED, NEUROENTER BIOL GRP, CURE DIG DIS RES CTR, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A705 EP A705 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702805 ER PT J AU Lembo, T Fullerton, S Mayer, EA AF Lembo, T Fullerton, S Mayer, EA TI Is pain the predominant symptom in irritable bowel syndrome (IBS)? SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, NEUROENTER BIOL GRP, CURE DIGEST DIS RES CTR, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A705 EP A705 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702803 ER PT J AU Lewis, JD Davidson, CD Davies, JK Kaplan, LM AF Lewis, JD Davidson, CD Davies, JK Kaplan, LM TI Expression of kinase-competent and kinase-deficient TrkC neurotrophin-3 receptors in rat enteric nervous system is tissue-specific and differentially regulated during gut development. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, COMBINED PROGRAM PEDIAT GI, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1093 EP A1093 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704352 ER PT J AU Lieberman, DA Ippoliti, AF Weber, LJ Weinstein, WM AF Lieberman, DA Ippoliti, AF Weber, LJ Weinstein, WM TI Long-term omeprazole is not associated with an increased incidence of colon neoplasia SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 PORTLAND VA MED CTR, DEPT MED, PORTLAND, OR USA. UNIV CALIF LOS ANGELES, DEPT MED, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A176 EP A176 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73700699 ER PT J AU Lukascewicz, G Abcouwer, S Souba, W AF Lukascewicz, G Abcouwer, S Souba, W TI Enhanced hepatic glutamine production during sepsis is adrenal gland-independent. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1401 EP A1401 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705573 ER PT J AU Mashimo, H Wu, C Fishman, MC Podolsky, DK AF Mashimo, H Wu, C Fishman, MC Podolsky, DK TI Protection and healing of intestinal mucosa: Gene-targeted disruption of intestinal trefoil factor impairs defense of mucosal integrity. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CARDIOVASC RES CTR, BOSTON, MA 02114 USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A959 EP A959 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703816 ER PT J AU Mayer, EA Munakata, J Mandelkern, M Hoh, K Kodner, A Naliboff, B Silverman, DHS AF Mayer, EA Munakata, J Mandelkern, M Hoh, K Kodner, A Naliboff, B Silverman, DHS TI Correlation of cortical and subcortical brain activation with autonomic responses to rectal stimuli in humans SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT PHYSIOL, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT NUCL MED, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, CURE, NEUROENTER BIOL GRP, LOS ANGELES, CA 90073 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A715 EP A715 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702845 ER PT J AU McAlindon, ME Gray, T Galvin, A Sewell, H Podolsky, DK Mahida, YR AF McAlindon, ME Gray, T Galvin, A Sewell, H Podolsky, DK Mahida, YR TI Numerous cells migrate out of the lamina propria (LP) of normal & inflammatory bowel disease (IBD) mucosa following loss of surface epithelial cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV NOTTINGHAM HOSP, DIV GASTROENTEROL, NOTTINGHAM, ENGLAND. UNIV NOTTINGHAM HOSP, DIV PATHOL, NOTTINGHAM, ENGLAND. UNIV NOTTINGHAM HOSP, DEPT IMMUNOL, NOTTINGHAM, ENGLAND. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A961 EP A961 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703825 ER PT J AU McCabe, RP Woody, J vanDeventer, S Targan, SR Mayer, L vanHogezand, R Rutgeerts, P Hanauer, SB Podolsky, D Elson, CO AF McCabe, RP Woody, J vanDeventer, S Targan, SR Mayer, L vanHogezand, R Rutgeerts, P Hanauer, SB Podolsky, D Elson, CO TI A multicenter trial of cA2 anti-TNF chimeric monoclonal antibody in patients with active Crohn's disease. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV ALABAMA, BIRMINGHAM, AL USA. UNIV AMSTERDAM, AMSTERDAM, NETHERLANDS. CEDARS SINAI MED CTR, LOS ANGELES, CA 90048 USA. MT SINAI MED CTR, NEW YORK, NY 10029 USA. ACAD ZICKENHUIS, LEIDEN, NETHERLANDS. UNIV CHICAGO, CHICAGO, IL 60637 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 0 TC 59 Z9 60 U1 1 U2 3 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A962 EP A962 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703828 ER PT J AU McCracken, JD Jacoby, RF Kantoci, D Murray, ED Wechter, WJ AF McCracken, JD Jacoby, RF Kantoci, D Murray, ED Wechter, WJ TI The effect of R-flurbiprofen on inhibition of polyp formation in the Min mouse model. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 LOMA LINDA UNIV, MED CTR, DIV GASTROENTEROL, LOMA LINDA, CA USA. LOMA LINDA UNIV, MED CTR, DEPT CHEM ENDOCRINOL, LOMA LINDA, CA USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53705 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A555 EP A555 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702208 ER PT J AU Meijssen, MAC Devaney, K Bhan, AK Podolsky, DK AF Meijssen, MAC Devaney, K Bhan, AK Podolsky, DK TI Altered cytokine and CD14 gene expression by intestinal epithelial cells of interleukin-2 deficient mice. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A966 EP A966 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703846 ER PT J AU Morales, V Polischuk, J Parkos, C Liang, T Russell, G Mizoguchi, A Bhan, A Blumberg, R AF Morales, V Polischuk, J Parkos, C Liang, T Russell, G Mizoguchi, A Bhan, A Blumberg, R TI Characterization of gp70 in intestinal epithelial cell (IEC)-intestinal intraepithelial lymphocyte (iIEL) interactions. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A972 EP A972 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703871 ER PT J AU Munakata, J Silverman, DHS Hoh, CK Mandelkern, MA Blahd, W Mayer, EA AF Munakata, J Silverman, DHS Hoh, CK Mandelkern, MA Blahd, W Mayer, EA TI Rectosigmoid sensitization correlates with thalamic response to rectal pain: An O-15-water PET study of normal subjects and IBS patients SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, MED CTR, DEPT MED, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, MED CTR, DEPT NUCL MED, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A720 EP A720 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702864 ER PT J AU Munakata, J Naliboff, B Mayer, EA AF Munakata, J Naliboff, B Mayer, EA TI Disease activity in IBS patients correlates with physiological alterations SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, CURE, NEUROENTER BIOL GRP, LOS ANGELES, CA 90024 USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT PHYSIOL, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, LOS ANGELES, CA 90024 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A720 EP A720 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702865 ER PT J AU Nakagawa, H Wang, T Odze, R Inomoto, T Zukerberg, L Wilson, J Rustgi, AK AF Nakagawa, H Wang, T Odze, R Inomoto, T Zukerberg, L Wilson, J Rustgi, AK TI Cyclin D1 oncogene overexpression in transgenic mice causes dysplasia in the esophagus and forestomach SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, GASTROINTESTINAL UNIT, BOSTON, MA USA. HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. UNIV GLASGOW, DEPT MOLEC BIOL, GLASGOW G61 1BD, LANARK, SCOTLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A566 EP A566 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702253 ER PT J AU Nakagawa, H Jenkins, TD Rustgi, AK AF Nakagawa, H Jenkins, TD Rustgi, AK TI Novel nuclear transcriptional factors interact with viral and cellular promoters in esophageal squamous epithelial cells SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, GASTROINTESTINAL UNIT, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A566 EP A566 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702251 ER PT J AU Nurko, S Thobani, S GarciaAranda, JA Isani, Z PerezPerez, G Blaser, M Snyder, J AF Nurko, S Thobani, S GarciaAranda, JA Isani, Z PerezPerez, G Blaser, M Snyder, J TI Does the presence of H-pylori affect the outcome during treatment for persistent diarrhea? SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HOSP INFANTIL MEXICO DR FEDERICO GOMEZ, DEPT PEDIAT, MEXICO CITY, DF, MEXICO. HOSP INFANTIL MEXICO DR FEDERICO GOMEZ, DEPT MED, MEXICO CITY, DF, MEXICO. VANDERBILT UNIV, NASHVILLE, TN 37240 USA. UNIV CALIF SAN FRANCISCO, SAN FRANCISCO, CA 94143 USA. MASSACHUSETTS GEN HOSP, COMBINED PROGRAM PEDIAT GASTROENTEROL, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A213 EP A213 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73700845 ER PT J AU Ogata, H Podolsky, DK AF Ogata, H Podolsky, DK TI Neurotransmitters regulate human intestinal trefoil peptide expression in intestinal epithelial cells SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. RI Ogata, Haruhiko/B-3964-2014 NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A983 EP A983 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703913 ER PT J AU Ouellette, AJ Hsieh, MM Selsted, ME AF Ouellette, AJ Hsieh, MM Selsted, ME TI Structure and function of cryptdins isolated from mouse small intestinal lumen. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. UNIV CALIF IRVINE, COLL MED, DEPT MICROBIOL & MOLEC GENET, IRVINE, CA 92717 USA. UNIV CALIF IRVINE, COLL MED, DEPT PATHOL, IRVINE, CA 92717 USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A985 EP A985 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703922 ER PT J AU Pack, M SolnicaKrezel, L Malicki, J Neuhauss, SCF Schier, AF Stemple, DL Driever, W Fishman, MC AF Pack, M SolnicaKrezel, L Malicki, J Neuhauss, SCF Schier, AF Stemple, DL Driever, W Fishman, MC TI Genetic approach to vertebrate digestive organ development using zebrafish. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, CARDIOVASC RES CTR, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, GI UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT MED, CAMBRIDGE, MA 02138 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A829 EP A829 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703297 ER PT J AU Parkos, CA Colgan, SP Diamond, MS Nusrat, A Liang, T Springer, TA Madara, JL AF Parkos, CA Colgan, SP Diamond, MS Nusrat, A Liang, T Springer, TA Madara, JL TI Expression and polarization of ICAM-1 on intestinal epithelia and it's consequences for CD11b/CD18 based interactions with neutrophils (PMN). SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. CTR BLOOD RES, DEPT PATHOL, BOSTON, MA 02115 USA. RI Nusrat, Asma/B-3887-2009; Parkos, Charles/B-3896-2009; Colgan, Sean/B-4573-2009 NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A987 EP A987 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703929 ER PT J AU Quinn, JJ Fusunyan, RD MacDermott, RP Sanderson, IR AF Quinn, JJ Fusunyan, RD MacDermott, RP Sanderson, IR TI Butyrate switches the pattern of chemokine secretion by intestinal epithelial cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 COLL HOLY CROSS, WORCESTER, MA 01610 USA. LAHEY CLIN FDN, GASTROINTESTINAL UNIT, BURLINGTON, MA USA. MASSACHUSETTS GEN HOSP, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, BOSTON, MA 02114 USA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A833 EP A833 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73703314 ER PT J AU Rattner, DW Freehan, ML AF Rattner, DW Freehan, ML TI Should laparoscopic nissen fundoplication be performed in obese patients? SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1411 EP A1411 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705615 ER PT J AU Reid, AE Xavier, R Cardiff, R Wang, T Liang, TJ AF Reid, AE Xavier, R Cardiff, R Wang, T Liang, TJ TI Transgenic expression of tpr-met oncogene leads to the development of hepatic hyperplasia and mammary tumors. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, GI UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, CAMBRIDGE, MA 02138 USA. UNIV CALIF DAVIS, SCH MED, DEPT PATHOL, DAVIS, CA 95616 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A582 EP A582 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702314 ER PT J AU Reinecker, HC MacDermot, RP Mirau, S Meijssen, MAC Dignass, AU Podolsky, DK AF Reinecker, HC MacDermot, RP Mirau, S Meijssen, MAC Dignass, AU Podolsky, DK TI Intestinal expression of IL-15 - Autocrine regulation of intestinal epithelial cell function. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. LAHEY CLIN FDN, BURLINGTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1110 EP A1110 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704422 ER PT J AU Ren, J Brunicardi, FC Seensalu, R Lloyd, KK Wu, SV Walsh, JH AF Ren, J Brunicardi, FC Seensalu, R Lloyd, KK Wu, SV Walsh, JH TI Occupation of somatostatin receptor 2A enhances CCK-A receptor mediated cAMP response in transfected HEK-293 cells SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 BAYLOR COLL MED, DEPT SURG, HOUSTON, TX 77035 USA. UNIV CALIF LOS ANGELES, DEPT MED, CURE DIGEST DIS RES CTR, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1111 EP A1111 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704426 ER PT J AU Rivera, J GraemeCook, F Werner, J Rattner, DW Rustgi, AK Warshaw, AL FernandezdelCastillo, C AF Rivera, J GraemeCook, F Werner, J Rattner, DW Rustgi, AK Warshaw, AL FernandezdelCastillo, C TI Pancreatic resection and the induction of ductal cancer in a rat model SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT SURG, BOSTON, MA USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT PATHOL, BOSTON, MA USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, GI UNIT, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1413 EP A1413 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705622 ER PT J AU Rogers, S Furusaka, A Liang, TJ AF Rogers, S Furusaka, A Liang, TJ TI Identification of cellular factors interacting with the preS2 domain of the surface protein of the hepatitis B virus: Implication for viral assembly and transactivation SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GI UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1305 EP A1305 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705195 ER PT J AU Rosenberg, IM Podolsky, DK AF Rosenberg, IM Podolsky, DK TI Epithelial cell kinase: Autocrine target regulated by divergent growth modulatory cytokines SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1113 EP A1113 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704432 ER PT J AU Rosenberg, IM Podolsky, DK AF Rosenberg, IM Podolsky, DK TI Hydrogen peroxide stimulates protein tyrosine phosphorylation in human intestinal epithelial cells. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR STUDY INFLAMMATORY BOWEL DIS, DEPT MED, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1113 EP A1113 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704434 ER PT J AU Sands, BE Podolsky, DK Tremaine, WJ Sandborn, WJ Rutgeerts, PJ Hanauer, SB Mayer, L Targan, SR DeWoody, KL Braakman, TAJ Woody, JN AF Sands, BE Podolsky, DK Tremaine, WJ Sandborn, WJ Rutgeerts, PJ Hanauer, SB Mayer, L Targan, SR DeWoody, KL Braakman, TAJ Woody, JN TI Chimeric monoclonal anti-tumor necrosis factor antibody (cA2) in the treatment of severe, steroid-refractory ulcerative colitis (UC). SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. MAYO CLIN, ROCHESTER, MN USA. ACAD HOSP GASTHUISBERG, LOUVAIN, BELGIUM. UNIV CHICAGO HOSP & CLIN, CHICAGO, IL USA. MT SINAI HOSP, NEW YORK, NY 10029 USA. CEDARS SINAI MED CTR, LOS ANGELES, CA USA. CENTOCOR INC, MALVERN, PA USA. NR 0 TC 44 Z9 45 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1008 EP A1008 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704013 ER PT J AU Seensalu, R Avedian, D Barbuti, R Song, M Walsh, JH AF Seensalu, R Avedian, D Barbuti, R Song, M Walsh, JH TI Disruption of the actin cytoskeleton by cytochalasin D releases gastrin from isolated canine G-cells in primary culture. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, DEPT MED, DIGEST DIS RES CTR, CURE, LOS ANGELES, CA 90024 USA. RI Barbuti, Ricardo /H-6277-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1117 EP A1117 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704449 ER PT J AU Seensalu, R Avedian, D Barbuti, R Pothoulakis, C Slice, L Song, M Lamont, JT Walsh, JH AF Seensalu, R Avedian, D Barbuti, R Pothoulakis, C Slice, L Song, M Lamont, JT Walsh, JH TI Rho proteins are involved in bombesin stimulated gastrin release from isolated canine G-cells in primary culture. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, DEPT MED, DIGEST DIS RES CTR, CURE, LOS ANGELES, CA 90024 USA. HARVARD UNIV, BETH ISRAEL HOSP, SCH MED, BOSTON, MA USA. RI Barbuti, Ricardo /H-6277-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1117 EP A1117 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704448 ER PT J AU Shiraki, K Takahashi, H AF Shiraki, K Takahashi, H TI Expression of Fas ligand in human colon cancers. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MGH, CTR CANC, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A592 EP A592 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702356 ER PT J AU Simon, FR Fortune, J Iwahashi, M Stevens, J Dahl, R Sutherland, E AF Simon, FR Fortune, J Iwahashi, M Stevens, J Dahl, R Sutherland, E TI Differential effect of chronic ethanol feeding on hepatic structure and gene expression in male and female rats. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV COLORADO, HSC, DENVER VAMC, HEPATOBILIARY RES CTR, DENVER, CO 80262 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1327 EP A1327 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705284 ER PT J AU Song, M Wong, H Ohning, G Walsh, JH AF Song, M Wong, H Ohning, G Walsh, JH TI Immunohistochemical localization of the gastrin/CCK-B receptor in the rat stomach SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, CURE, DIGEST DIS RES CTR, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 14 Z9 14 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1120 EP A1120 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704462 ER PT J AU Tanaka, S Guth, PH Kaunitz, JD AF Tanaka, S Guth, PH Kaunitz, JD TI In vivo microscopic study of esophageal mucus gel thickness and blood flow during luminal acid challenge in rats SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, CURE, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A274 EP A274 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701090 ER PT J AU Tanaka, S Guth, PH Kaunitz, JD AF Tanaka, S Guth, PH Kaunitz, JD TI Pentagastrin enhancement of gastric mucosal defenses is related to H-2 receptor activation but not acid SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, CURE, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A274 EP A274 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701089 ER PT J AU Tanaka, S Podolsky, DK Guth, PH Kaunitz, JD AF Tanaka, S Podolsky, DK Guth, PH Kaunitz, JD TI Gastroprotective effect of human spasmolytic polypeptide (HSP): Effect on mucus acid permeation SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, DEPT MED, LOS ANGELES, CA 90073 USA. MASSACHUSETTS GEN HOSP, GI UNIT, BOSTON, MA 02114 USA. UNIV CALIF LOS ANGELES, SCH MED, LOS ANGELES, CA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A273 EP A273 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701087 ER PT J AU Tearney, GJ Brezinski, ME Bouma, BE Southern, JF Fujimoto, JG AF Tearney, GJ Brezinski, ME Bouma, BE Southern, JF Fujimoto, JG TI High resolution imaging of gastrointestinal tissue using optical coherence tomography. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MIT, DEPT ELECT ENGN & COMP SCI, ELECTR RES LAB, CAMBRIDGE, MA 02139 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A478 EP A478 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701903 ER PT J AU Togawa, K Yan, TX Rustgi, AK AF Togawa, K Yan, TX Rustgi, AK TI A serine-threonine kinase localizes to intestinal crypt cells and is regulated by epidermal growth factor. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, GASTROINTESTINAL UNIT, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A604 EP A604 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702403 ER PT J AU Torres, C Turner, G Rustgi, AK Wang, H Shahsafaei, A Odze, R AF Torres, C Turner, G Rustgi, AK Wang, H Shahsafaei, A Odze, R TI E-cadherin expression in esophageal squamous cell carcinoma: Correlation with survival SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, BETH ISRAEL HOSP, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, GASTROINTESTINAL UNIT, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A604 EP A604 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73702404 ER PT J AU Wang, TC Koh, TJ Varro, A Cahill, R Fox, JG Dockray, GJ AF Wang, TC Koh, TJ Varro, A Cahill, R Fox, JG Dockray, GJ TI Processing and functional significance of human progastrin in transgenic mice. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MIT, DIV COMPARAT MED, CAMBRIDGE, MA 02139 USA. UNIV LIVERPOOL, PHYSIOL LAB, LIVERPOOL, MERSEYSIDE, ENGLAND. RI Varro, Andras/M-2647-2016 OI Varro, Andras/0000-0003-0745-3603 NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1132 EP A1132 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704507 ER PT J AU Wang, TC Andrutis, K Li, XT Cahill, R Rustgi, AK Fox, JG AF Wang, TC Andrutis, K Li, XT Cahill, R Rustgi, AK Fox, JG TI Cooperation of Helicobacter felis infection with nitrosamines and genetic factors in inducing gastric proliferation in mice. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MIT, DIV COMPARAT MED, CAMBRIDGE, MA 02139 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1042 EP A1042 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704150 ER PT J AU Werner, J Rivera, J Lewandrowski, K Adrie, C Rattner, DW FernandezdelCastillo, C Warshaw, AL AF Werner, J Rivera, J Lewandrowski, K Adrie, C Rattner, DW FernandezdelCastillo, C Warshaw, AL TI Differing roles of nitric oxide (NO) in the pathogenesis of acute edematous versus necrotizing pancreatitis SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT ANESTHESIOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1425 EP A1425 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705671 ER PT J AU Werner, J Saghir, M Laposata, M Rattner, DW Warshaw, AL FernandezdelCastillo, C AF Werner, J Saghir, M Laposata, M Rattner, DW Warshaw, AL FernandezdelCastillo, C TI Fatty acid ethyl esters may mediate alcohol-induced pancreatic injury. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A441 EP A441 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701756 ER PT J AU Wong, DKH Dudley, D Afdhal, N Rice, C Houghton, M Walker, BD Koziel, MJ AF Wong, DKH Dudley, D Afdhal, N Rice, C Houghton, M Walker, BD Koziel, MJ TI Liver-derived cytotoxic T lymphocytes in non-resolving hepatitis C infection. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. BOSTON CITY HOSP, BOSTON, MA 02118 USA. WASHINGTON UNIV, ST LOUIS, MO 63130 USA. CHIRON CORP, EMERYVILLE, CA 94608 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1361 EP A1361 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705421 ER PT J AU Wong, DKH Koziel, MJ Dudley, D Afdhal, N Rice, C Houghton, M Walker, BD AF Wong, DKH Koziel, MJ Dudley, D Afdhal, N Rice, C Houghton, M Walker, BD TI Hepatitis C virus-specific cytotoxic T lymphocytes from liver and peripheral blood. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. BOSTON CITY HOSP, BOSTON, MA 02118 USA. WASHINGTON UNIV, ST LOUIS, MO 63130 USA. CHIRON CORP, EMERYVILLE, CA 94608 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1361 EP A1361 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705419 ER PT J AU Wu, DC Mashimo, H Fishman, MC Podolsky, DK AF Wu, DC Mashimo, H Fishman, MC Podolsky, DK TI Spasmolytic polypeptide and mucin glycoprotein induction in ITF knock-out mice after oral dextran sulfate SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, CARDIOVASC RES CTR, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, CTR STUDY INFLAMMATORY BOWEL DIS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A298 EP A298 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701188 ER PT J AU Wu, SV Yang, M Seensalu, R McRoberts, J Walsh, JH AF Wu, SV Yang, M Seensalu, R McRoberts, J Walsh, JH TI First intracellular loop of CCK-A receptor is essential for cAMP response to CCK in transfected HEK-293 cells SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, CTR ULCER RES & EDUC, DEPT MED, DIGEST DIS RES CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1133 EP A1133 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704512 ER PT J AU Yang, H Hocker, M Tache, Y Wong, H Wang, T AF Yang, H Hocker, M Tache, Y Wong, H Wang, T TI Fundic histidine decarboxylase (HDC) gene expression is stimulated by central TRH-induced cholinergic vagal activation. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. UNIV CALIF LOS ANGELES, VET ADM MED CTR, DEPT MED, CURE DIGEST DIS RES CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A301 EP A301 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701199 ER PT J AU Yang, HT Walsh, JH Wang, YH Wang, JD Zhou, N Zhou, DY Wu, SV AF Yang, HT Walsh, JH Wang, YH Wang, JD Zhou, N Zhou, DY Wu, SV TI High prevalence of cag positive genotype in H-pylori isolates from Chinese subjects SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 NANFANG HOSP, GUANGZHOU, PEOPLES R CHINA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, CURE DIGEST DIS RES CTR, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, BRI, LOS ANGELES, CA 90073 USA. W LOS ANGELES VET AFFAIRS MED CTR, LOS ANGELES, CA 90073 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A302 EP A302 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73701204 ER PT J AU Yoo, K Chung, RT Kaplan, LM AF Yoo, K Chung, RT Kaplan, LM TI RNA-dependent RNA polymerase activity of NS5B from a strain of HCV associated with fulminant hepatitis and elevated circulating RNA levels. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1366 EP A1366 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73705441 ER PT J AU Zhang, ZS Hocker, M Koh, TJ Wang, TC AF Zhang, ZS Hocker, M Koh, TJ Wang, TC TI The human histidine decarboxylase (HDC) promoter is regulated by gastrin and phorbol ester through a downstream cis-acting element. SO GASTROENTEROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1996 VL 110 IS 4 SU S BP A1137 EP A1137 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF737 UT WOS:A1996UF73704527 ER PT J AU Jensen, DM Kovacs, TOG Jutabha, R Machicado, GA Savides, T Smith, J AF Jensen, DM Kovacs, TOG Jutabha, R Machicado, GA Savides, T Smith, J TI A safe and effective technique for endoscopic removal of adherent clots from GI lesions: Cold guillotining after epinephrine injection. SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,DIGEST DIS RES CTR,CURE,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA. RI smith, james/C-9922-2016 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1996 VL 43 IS 4 BP 25 EP 25 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UH281 UT WOS:A1996UH28100025 ER PT J AU Jutabha, R Jensen, DM Machicado, G Hirabayashi, K AF Jutabha, R Jensen, DM Machicado, G Hirabayashi, K TI Reliability of endoscopic ultrasound probe imaging of canine abdominal veins before and after sclerotherapy in a blinded study. SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,MED CTR,W LOS ANGELES VET AFFAIRS MED CTR,DIGEST DIS RES CTR,CURE,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1996 VL 43 IS 4 BP 26 EP 26 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UH281 UT WOS:A1996UH28100026 ER PT J AU Dea, SK Chin, PC AF Dea, SK Chin, PC TI Clinical outcomes of early feeding after percutaneous endoscopic gastrostomy (PEG) placement: A randomized controlled trial. SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1996 VL 43 IS 4 BP 234 EP 234 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UH281 UT WOS:A1996UH28100234 ER PT J AU Jensen, DM Kovacs, TOG Jutabha, R Savides, T Cheng, S Jensen, ME Machicado, GA King, J Gornbein, J Smith, J AF Jensen, DM Kovacs, TOG Jutabha, R Savides, T Cheng, S Jensen, ME Machicado, GA King, J Gornbein, J Smith, J TI Initial results of a multicenter, randomized controlled trial (RCT) of medical vs combination (Combo) endoscopic therapy for prevention of recurrent severe ulcer hemorrhage from non-bleeding adherent clots. SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CURE,DIGEST DIS RES CTR,LOS ANGELES,CA. ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA. RI smith, james/C-9922-2016 NR 0 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1996 VL 43 IS 4 BP 245 EP 245 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UH281 UT WOS:A1996UH28100245 ER PT J AU Schapiro, GD Jaffe, D Ryder, D Brugge, W Kelsey, PB Schapiro, RH AF Schapiro, GD Jaffe, D Ryder, D Brugge, W Kelsey, PB Schapiro, RH TI Wire guided papillotomes increase the selective bile duct cannulation rate. SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1996 VL 43 IS 4 BP 416 EP 416 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UH281 UT WOS:A1996UH28100416 ER PT J AU Quirk, D Rattner, D Fernandez, C Warshaw, A Brugge, W AF Quirk, D Rattner, D Fernandez, C Warshaw, A Brugge, W TI The use of endoscopic ultrasonography to reduce the cost of treating ampullary tumors. SO GASTROINTESTINAL ENDOSCOPY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD APR PY 1996 VL 43 IS 4 BP 553 EP 553 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UH281 UT WOS:A1996UH28100553 ER PT J AU Hofmann, F Livingston, DM AF Hofmann, F Livingston, DM TI Differential effects of cdk2 and cdk3 on the control of pRb and E2F function during G(1) exit SO GENES & DEVELOPMENT LA English DT Article DE cdk2; cdk3; E2F; pRb; cell cycle control ID RETINOBLASTOMA SUSCEPTIBILITY GENE; CYCLIN-DEPENDENT KINASES; CELL-CYCLE; COMPLEX-FORMATION; PRODUCT; PROTEIN; BINDING; SV40; FAMILY; TRANSFORMATION AB The cyclin-dependent kinases cdk2 and cdk3 are required for the G(1)-S transition in mammalian cells. Here we show that G(1) arrest induced by the corresponding dominant-negative mutants of these enzymes, cdk2dn or cdk3dn, is resistant to the action of SV40 T antigen (T). In the presence of cdk2dn, T released active E2F from negative control by pRb and its related family members (pocket proteins) but failed to induce S-phase. Therefore, among other targets, cdk2 also phosphorylates nonpocket protein substrates in promoting S-phase entry, and T does not mimic all cdk2 functions. In the presence of cdk3dn, however, T failed to induce cell cycle progression or stimulate E2F-dependent transcription activity. Dominant-negative cdk3 inhibited E2F-1, E2F-2, and, less significantly, E2F-3, but not E2F-4 transcription activity. The inhibition occurred in a pRb-independent manner and did not affect the DNA-binding capacity of the transcription factor. Cdk3 bound specifically to E2F-1/DP-1 complexes in vivo, most likely through DP-1. Thus, cdk3 function contributes to the activation of E2F-1, E2F-2, and partially, E2F-3 and, thereby, participates in the process of S-phase entry. C1 DANA FARBER CANC INST,DIV NEOPLAST DIS MECH,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 37 TC 80 Z9 81 U1 0 U2 2 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD APR 1 PY 1996 VL 10 IS 7 BP 851 EP 861 DI 10.1101/gad.10.7.851 PG 11 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA UE558 UT WOS:A1996UE55800007 PM 8846921 ER PT J AU Haines, JL Pritchard, ML Saunders, AM Schildkraut, JM Growdon, JH Gaskell, PC Farrer, LA Auerbach, SA Gusella, JF Locke, PA Rosi, BL Yamaoka, L Small, GW Conneally, PM Roses, AD PericakVance, MA AF Haines, JL Pritchard, ML Saunders, AM Schildkraut, JM Growdon, JH Gaskell, PC Farrer, LA Auerbach, SA Gusella, JF Locke, PA Rosi, BL Yamaoka, L Small, GW Conneally, PM Roses, AD PericakVance, MA TI No genetic effect of alpha(1)-antichymotrypsin in Alzheimer disease SO GENOMICS LA English DT Article ID APOLIPOPROTEIN-E; AMYLOID DEPOSITS; TYPE-4 ALLELE; ALPHA-1-ANTICHYMOTRYPSIN; PROTEIN; LINKAGE AB Alzheimer disease (AD) is the most common neurodegenerative disorder for individuals over the age of 40. AD has a complex etiology, and it is likely that multiple genes, acting independently and/or interacting, affect the risk of developing AD. Several genes involved with AD have been described already, but only the APOE gene on chromosome 19q has been shown to affect the risk of the common late onset form of AD. alpha(1)-Antichymotrypsin (AACT) is a major component of the amyloid plaques found in the brains of AD patients, and an allele in its gene has been proposed to increase the risk of developing AD when also associated with the APOE-4 allele. We have examined the role of this AACT polymorphism in a large set of families and sporadic cases, and do not see any effect, either alone or in combination with the APOE-4 allele. (C) 1996 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. DUKE UNIV,MED CTR,DEPT MED,DIV NEUROL,DURHAM,NC 27710. DUKE UNIV,MED CTR,DUKE COMPREHENS CANC CTR,DURHAM,NC 27710. BOSTON UNIV,MED CTR,DEPT NEUROL,BOSTON,MA. UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. INDIANA UNIV,MED CTR,DEPT MED & MOLEC GENET,INDIANAPOLIS,IN. RP Haines, JL (reprint author), MASSACHUSETTS GEN HOSP,MOL NEUROGENET UNIT,BLDG 149,6TH FLOOR,BOSTON,MA 02129, USA. RI Haines, Jonathan/C-3374-2012; OI Farrer, Lindsay/0000-0001-5533-4225 FU NIA NIH HHS [AG05134, U24 AG021886]; NINDS NIH HHS [NS26630, NS531153] NR 18 TC 89 Z9 89 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR 1 PY 1996 VL 33 IS 1 BP 53 EP 56 DI 10.1006/geno.1996.0158 PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA UF102 UT WOS:A1996UF10200006 PM 8617509 ER PT J AU Goodman, A Zukerberg, LR Rice, LW Fuller, AF Young, RH Scully, RE AF Goodman, A Zukerberg, LR Rice, LW Fuller, AF Young, RH Scully, RE TI Squamous cell carcinoma of the endometrium: A report of eight cases and a review of the literature SO GYNECOLOGIC ONCOLOGY LA English DT Article ID STAGE-I; CANCER AB Background: Endometrial squamous cell carcinoma is extremely rare, with only 56 cases reported in the literature. Methods: Six cases of endometrial squamous cell carcinoma were found in a review of 1182 cases of uterine corpus cancer treated at the Massachusetts General Hospital from 1975 to 1993, Two additional cases were seen in pathological consultation. The clinicopathological features of these 8 cases and the 56 reported cases were analyzed. Results: The average age of the patients was 67 years; almost all of them were postmenopausal. The most frequent presenting symptom was vaginal bleeding. Chronic pyometra and nulliparity were predisposing factors. The average duration of symptoms before diagnosis was 11.5 months. Total abdominal hysterectomy with bilateral salpingo-oophorectomy was the primary treatment in 58 patients. Eighty percent of the patients with Stage I tumors survived; the median follow-up time was 32 months. The survival rate for patients with Stage III tumors was only 20%, and all 6 patients with Stage IV disease died. Conclusions: The preoperative diagnosis of endometrial squamous cell carcinoma may be difficult, since curettage specimens may show only highly differentiated squamous epithelium. The strong relationship between tumor stage and survival suggests that early diagnosis and treatment are imperative. (C) 1996 Academic Press, Inc. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. UNIV VIRGINIA,DEPT OBSTET & GYNECOL,CHARLOTTESVILLE,VA 22903. RP Goodman, A (reprint author), MASSACHUSETTS GEN HOSP,DEPT OBSTET & GYNECOL,WANG AMBULATORY CARE CTR,BOSTON,MA 02114, USA. NR 55 TC 35 Z9 40 U1 1 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD APR PY 1996 VL 61 IS 1 BP 54 EP 60 DI 10.1006/gyno.1996.0096 PG 7 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA UC961 UT WOS:A1996UC96100011 PM 8626118 ER PT J AU Biggs, PJ AF Biggs, PJ TI Obliquity factors for Co-60 and 4, 10, and 18 MV x rays for concrete, steel, and lead and angles of incidence between 0 degrees and 70 degrees SO HEALTH PHYSICS LA English DT Article DE bremsstrahlung; x rays; radiation, medical; Co-60 AB The attenuation of Co-60 gamma rays and photons of 4, 10, and 18 MV x-ray beams by concrete, steel, and lead has been studied using the Monte Carlo technique for angles of incidence 0 degrees, 30 degrees, 45 degrees, 60 degrees, and 70 degrees. Transmission factors have been determined down to < 2 x 10(-5) in all cases. The results show that deviation from the obliquity factor increases with angle but is not significant for angles less than or equal to 45 degrees, At 70 degrees angle of incidence and a transmission factor of 10(-5), the obliquity factor varies between 1.2 and 1.9 for concrete, between 1.4 and 1.7 for steel, and between 1.4 and 1.5 for lead for the range of energies investigated. This amounts to an additional 86 and 50 cm of concrete, 25 and 23 cm of steel, and 8 and 14 cm of lead for Co-60 and 18 MV x rays, respectively, The results for Co-60 in concrete and lead are in good agreement with previously published experimental work. Fits to the data using mathematical models allow reconstruction of all data curves to better than 1% on average and 7% in the worst single case. RP Biggs, PJ (reprint author), HARVARD UNIV, SCH MED, MASSACHUSETTS GEN HOSP, DEPT RADIAT ONCOL, BOSTON, MA 02114 USA. NR 9 TC 8 Z9 8 U1 0 U2 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PD APR PY 1996 VL 70 IS 4 BP 527 EP 536 DI 10.1097/00004032-199604000-00010 PG 10 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA UA703 UT WOS:A1996UA70300010 PM 8617593 ER PT J AU Melcher, JR Knudson, IM Fullerton, BC Guinan, JJ Norris, BE Kiang, NYS AF Melcher, JR Knudson, IM Fullerton, BC Guinan, JJ Norris, BE Kiang, NYS TI Generators of the brainstem auditory evoked potential in cat .1. An experimental approach to their identification SO HEARING RESEARCH LA English DT Article DE cochlear nucleus; superior olivary complex; kainic acid; lesion ID SUPERIOR OLIVARY COMPLEX; KAINIC ACID LESIONS; ANTEROVENTRAL COCHLEAR NUCLEUS; LATERAL GENICULATE-NUCLEUS; RAT INFERIOR COLLICULUS; INDUCED NEURONAL LOSS; STEM RESPONSES; TONOTOPIC ORGANIZATION; HORSERADISH-PEROXIDASE; BINAURAL RESPONSES AB This paper is the first in a series aimed at identifying the cellular generators of the brainstem auditory evoked potential (BAEP) in cats. The approach involves (1) developing experimental procedures for making small selective lesions and determining the corresponding changes in BAEP waveforms, (2) identifying brainstem regions involved in BAEP generation by examining the effects of lesions on the BAEP and, (3) identifying specific cell populations involved by combining the lesion results with electrophysiological and anatomical information from other kinds of studies. We created lesions in the lower brainstem by injecting kainic acid which is generally toxic for neuronal cell bodies but not for axons and terminals. This first paper describes the justifications for using kainic acid, explains the associated problems, and develops a methodology that addresses the main difficulties. The issues and aspects of the specific methods are generally applicable to physiological and anatomical studies using any neurotoxin, as well as to the present BAEP study. The methods chosen involved (1) measuring the BAEP at regular intervals until it reached a post-injection steady state and perfusing the animals with fixative shortly after the last BAEP recordings were made, (2) using objective criteria to distinguish injection-related BAEP changes from unrelated ones, (3) making control injections to identify effects not due to kainic acid toxicity, (4) verifying the anatomical and functional integrity of axons in lesioned regions, and (5) examining injected brainstems microscopically for cell loss and cellular abnormalities indicating dysfunction, This combination of methods enabled us to identify BAEP changes which are clearly correlated with lesion locations. C1 MIT,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Melcher, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [P01 DC000119-24, T32DC00006, P01DC00119] NR 73 TC 36 Z9 36 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1996 VL 93 IS 1-2 BP 1 EP 27 DI 10.1016/0378-5955(95)00178-6 PG 27 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500001 PM 8735066 ER PT J AU Melcher, JR Guinan, JJ Knudson, IM Kiang, NYS AF Melcher, JR Guinan, JJ Knudson, IM Kiang, NYS TI Generators of the brainstem auditory evoked potential in cat .2. Correlating lesion sites with waveform changes SO HEARING RESEARCH LA English DT Article DE cochlear nucleus; superior olivary complex; kainic acid; lesion ID SUPERIOR OLIVARY COMPLEX; BUSHY CELL AXONS; ANTEROVENTRAL COCHLEAR NUCLEUS; DORSAL LATERAL GENICULATE; INDUCED NEURONAL LOSS; KAINIC ACID; STEM RESPONSES; HORSERADISH-PEROXIDASE; EFFERENT PROJECTIONS; INFERIOR COLLICULUS AB Brainstem regions involved in generating the brainstem auditory evoked potential (BAEP) were identified by examining the effects of lesions on the click-evoked BAEP in cats. An excitotoxin, kainic acid, was injected into various parts of the cochlear nucleus (CN) or into the superior olivary complex (SOC), The locations of the resulting lesions were correlated with the changes produced in the various extrema of the BAEP waveforms, The results indicate that: (1) the earliest BAEP extrema (P1, N1 (recorded between vertex and the earbar ipsilateral to the stimulus) and P1a, P1b, (vertex to contralateral earbar)) are generated by cells with somata peripheral to the CN; (2) P2 is primarily generated by posterior anteroventral CN (AVCNp) and anterior posteroventral CN (PVCNa) cells; (3) SOC, anterior anteroventral CN (AVCNa), AVCNp, and PVCNa cells are involved in generating P3; (4) AVCNa cells are the main CN cells involved in P4, N4, and P5 generation; (5) both ipsilateral and contralateral SOC cells have a role in generating monaurally evoked P4 and P5; and (6) P5 is generated by cells with characteristic frequencies below 10 kHz. From (2) and (4), it is clear that P2 and P4-P5 are generated by cells in distinct, parallel pathways. C1 MIT,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Melcher, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [P01DC00119, T32DC00006, P01 DC000119-24] NR 46 TC 49 Z9 49 U1 0 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1996 VL 93 IS 1-2 BP 28 EP 51 DI 10.1016/0378-5955(95)00179-4 PG 24 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500002 PM 8735067 ER PT J AU Melcher, JR Kiang, NYS AF Melcher, JR Kiang, NYS TI Generators of the brainstem auditory evoked potential in cat .3. Identified cell populations SO HEARING RESEARCH LA English DT Article DE cochlear nucleus; superior olivary complex; spherical cell; globular cell ID ANTEROVENTRAL COCHLEAR NUCLEUS; SUPERIOR OLIVARY COMPLEX; INDUCED NEURONAL LOSS; SINGLE UNIT-ACTIVITY; STEM RESPONSES ABRS; TRAPEZOID BODY; MEDIAL NUCLEUS; INFERIOR COLLICULUS; HORSERADISH-PEROXIDASE; LATERAL LEMNISCUS AB This paper examines the relationship between different brainstem cell populations and the brainstem auditory evoked potential (BAEP), First, we present a mathematical model relating the BAEP to underlying cellular activity, Then, we identify specific cellular generators of the click-evoked BAEP in cats by combining model-derived insights with key experimental data. These data include (a) a correspondence between particular brainstem regions and specific extrema in the BAEP waveform, determined from lesion experiments, and (b) values for model parameters derived from published physiological and anatomical information, Ultimately, we conclude (with varying degrees of confidence) that: (1) the earliest extrema in the BAEP are generated by spiral ganglion cells, (2) P2 is mainly generated by cochlear nucleus (CN) globular cells, (3) P3 is partly generated by CN spherical cells and partly by cells receiving inputs from globular cells, (4) P4 is predominantly generated by medial superior olive (MSG) principal cells, which are driven by spherical cells, (5) the generators of P5 are driven by MSO principal cells, and (6) the BAEP, as a whole, is generated mainly by cells with characteristic frequencies above 2 kHz, Thus, the BAEP in cats mainly reflects cellular activity in two parallel pathways, one originating with globular cells and the other with spherical cells, Since the globular cell pathway is poorly represented in humans, we suggest that the human BAEP is largely generated by brainstem cells in the spherical cell pathway. Given our conclusions, it should now be possible to relate activity in specific cell populations to psychophysical performance since the BAEP can be recorded in behaving humans and animals. C1 MIT,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Melcher, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [T32DC00006, P01 DC000119-24, P01DC00119] NR 109 TC 105 Z9 107 U1 0 U2 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1996 VL 93 IS 1-2 BP 52 EP 71 DI 10.1016/0378-5955(95)00200-6 PG 20 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500003 PM 8735068 ER PT J AU Rosbe, KW Burgess, BJ Glynn, RJ Nadol, JB AF Rosbe, KW Burgess, BJ Glynn, RJ Nadol, JB TI Morphologic evidence for three cell types in the human spiral ganglion SO HEARING RESEARCH LA English DT Article DE spiral ganglion; human; morphometry ID NEURONS; COCHLEA; FIBERS; NERVE AB Although two types of spiral ganglion cells (large type I and smaller type II) have classically been described by anatomic studies in both animal and human spiral ganglion, there is physiologic and morphologic evidence for subtypes of the large type I ganglion cell. In addition, in the animal and human, a variety of morphologic differences based on cytoplasmic content, myelinization, immunostaining and morphometric analysis have suggested more than one variety of type I ganglion cell. Light and electron microscopic serial sections of the spiral ganglion in two human specimens in the basal, middle and upper middle turns were pooled for morphometric analysis of the cell area, nuclear area and axon diameter. Analysis of variance, bivariate scatter plots and multivariate cluster analysis provided evidence for 3 types of ganglion cells in the human spiral ganglion: large, intermediate and small, varying from each other significantly on the basis of cell area. It was suggested, based on the morphologic findings and prevalence of the cell types, that the large and intermediate cells were subtypes of the classic type I spiral ganglion cell, whereas the small ganglion cell was consistent with the classically described type II ganglion cell. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. FU NIDCD NIH HHS [R01 DC00152] NR 16 TC 19 Z9 20 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD APR PY 1996 VL 93 IS 1-2 BP 120 EP 127 DI 10.1016/0378-5955(95)00208-1 PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA UL655 UT WOS:A1996UL65500008 PM 8735073 ER PT J AU Kim, SK Demetri, GD AF Kim, SK Demetri, GD TI Chemotherapy and neutropenia SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID COLONY-STIMULATING FACTOR; BONE-MARROW TRANSPLANTATION; HIGH-DOSE CHEMOTHERAPY; FACTOR GM-CSF; NON-HODGKINS-LYMPHOMA; HEMATOPOIETIC PROGENITOR CELLS; CYTO-TOXIC AGENTS; CONTROLLED TRIAL; GROWTH-FACTOR; STEM-CELLS AB Myelosuppression is the most common toxicity associated with the administration of dose-intensive cytotoxic chemotherapy. The basic understanding of neutrophil biology and the physiology of chemotherapy-induced neutropenia has advanced tremendously in the past 2 decades. Concordantly, the ability to reduce the morbidity associated with neutropenia has improved. Adjunctive cytokine and progenitor cell support of hematologic recovery after myelosuppressive therapy have proved to be models of translational research and have led to novel therapeutic initiatives for patients with cancer and hematologic malignancies. In this article, fundamental aspects of neutrophil production are discussed, and the clinical development of hematopoietic cytokines active on cells of the leukocyte lineages is presented. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV MED ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. NR 123 TC 23 Z9 25 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8588 J9 HEMATOL ONCOL CLIN N JI Hematol. Oncol. Clin. North Am. PD APR PY 1996 VL 10 IS 2 BP 377 EP & DI 10.1016/S0889-8588(05)70344-0 PG 20 WC Oncology; Hematology SC Oncology; Hematology GA UC649 UT WOS:A1996UC64900006 PM 8707761 ER PT J AU Harper, SE Dienstag, JL AF Harper, SE Dienstag, JL TI Can interferon alfa treatment prevent hepatocellular carcinoma in patients with chronic hepatitis C infection and compensated cirrhosis? SO HEPATOLOGY LA English DT Article AB Patients with chronic active hepatitis C and cirrhosis often develop hepatocellular carcinoma. Interferon (IFN) seems to be effective in some patients but whether it prevents carcinogenesis is unknown. In a prospective randomised trial, we evaluated the effects of IFN-alpha in cirrhotic patients with HCV infection because of their high risk of hepatocellular carcinoma. 90 patients with compensated chronic active hepatitis C with cirrhosis were randomly allocated to receive IFN-alpha (6 MU three times weekly for 12-24 weeks) (45 patients) or symptomatic treatment (45 controls), and were followed up for 2-7 years. In nine controls, alanine aminotransferase (ALT) decreased to less than 80 IU/L but did not stay in the normal range. In 19 patients given IFN-alpha, ALT decreased to less than 80 IU/L (in seven patients,it became and stayed normal; P=0.011. Wilcoxon rank sum test). However, the mean change in ALT was not significantly different between the two groups. The mean change in peak alpha-fetoprotein values was smaller in patients given IFN-alpha than in controls (P=0.021). The mean change in the serum albumin level was higher in the IFN-alpha (P<0.001). The histological activity index in the 12 IFN-alpha paatients undergoing a second biopsy after therapy was improved (P=0.031). Hepatitis C viral RNA disappeared in seven (16%) of the 45 IFN-alpha patients (95% Cl, 7-29%)and in some of the 45 controls(0-8%, P=0.018). Hepatocellular carcinoma was detected in two (4%, 1-15%) IFN-alpha patients and 17 (38%, 24-54%) controls(P=0.002, Wilcoxon signed-rank test). The risk ratio of IFN-alpha treaatment versus symptomatic treatment was 0.067 (0.009.0.530; P=0.010 Cox's proportional hazards). Ifn-alpha improved liver function in chronic active hepatitis C with cirrhosis, and its use was associated with a decreased incidence of hepatocellular carcinoma. RP Harper, SE (reprint author), MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114, USA. NR 19 TC 17 Z9 17 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD APR PY 1996 VL 23 IS 4 BP 930 EP 933 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UF096 UT WOS:A1996UF09600039 PM 8666352 ER PT J AU Brown, D Lydon, J McLaughin, M StuartTilley, A Tyszkowski, R Alper, S AF Brown, D Lydon, J McLaughin, M StuartTilley, A Tyszkowski, R Alper, S TI Antigen retrieval in cryostat tissue sections and cultured cells by treatment with sodium dodecyl sulfate (SDS) SO HISTOCHEMISTRY AND CELL BIOLOGY LA English DT Article ID VACUOLAR H+-ATPASE; RAT-KIDNEY; WATER CHANNEL; INTERCALATED CELLS; BRUSH-BORDER; MEMBRANE; LOCALIZATION; CAVEOLAE; MICRODOMAINS; EXPRESSION AB A simple method for antigen retrieval in tissue sections and cell cultures is described. Because many antibodies recognize denatured proteins on western blots, but are poorly reactive by immunocytochemistry, the effect of applying sodium dodecyl sulfate (SDS) to cryostat sections of tissues and to cell cultures prior to immunostaining was examined. In many cases, a 5-min pretreatment with 1% SDS produced a dramatic increase in staining intensity by indirect immunofluorescence. Among the antibodies tested that showed a positive effect of SDS were an anti-Na/K-ATPase monoclonal antibody, an anti-AE1/2 anion exchanger polyclonal antipeptide antibody, a monoclonal anti-caveolin antibody, and an anti-rab4 monoclonal antibody. In other cases, including antibodies against gp330, aquaporin 1, and aqua porin 2, no effect of SDS was detected. The results show that SDS treatment can be used as a simple method of antigen retrieval in cryostat sections and on cultured cells. In some cases, antigens were not detectable without pretreatment with SDS. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP EAST,SCH MED,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP EAST,RENAL UNIT,BOSTON,MA 02129. BETH ISRAEL HOSP,MOLEC MED UNIT,BOSTON,MA 02215. BETH ISRAEL HOSP,RENAL UNIT,BOSTON,MA 02215. FU NIDDK NIH HHS [DK 42956, DK 43495] NR 28 TC 252 Z9 252 U1 0 U2 5 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-5564 J9 HISTOCHEM CELL BIOL JI Histochem. Cell Biol. PD APR PY 1996 VL 105 IS 4 BP 261 EP 267 DI 10.1007/BF01463929 PG 7 WC Cell Biology; Microscopy SC Cell Biology; Microscopy GA UF562 UT WOS:A1996UF56200002 PM 9072183 ER PT J AU Bornstein, SR Brown, JW Carballeira, A Goodman, J Scherbaum, WA Fishman, LM AF Bornstein, SR Brown, JW Carballeira, A Goodman, J Scherbaum, WA Fishman, LM TI Ultrastructural dynamics of mitochondrial morphology in varying functional forms of human adrenal cortical adenoma SO HORMONE AND METABOLIC RESEARCH LA English DT Article DE human; mitochondria; electron microscopy; ultrastructure; adrenal cortex; adrenal adenoma; cortisol; aldosterone; progesterone; infertility; Cushing's syndrome; Conn's syndrome ID CORTICOTROPIN-RELEASING HORMONE AB Adrenal cortical mitochondria display an extensive capacity to adapt morphologically to the functional state of the adrenal cortical cell. In the present study, we have used transmission electron microscopy to analyze cortical tissues from 3 normal human adrenal glands (zona fasciculata and zona glomerulosa), and from 8 steroid-secreting adrenal cortical adenomas (3 cortisol-producing, 4 aldosterone-producing, and 1 progesterone-producing tumor), correlating both clinical and biochemical features with cellular ultrastructure. The morphology of mitochondria was related to the enzyme activity and steroid-biosynthetic capacity of each tumor, Cells from aldosterone-producing adenomas demonstrated a large number of elongated tubular mitochondria with characteristic bridging of inner membranes, producing a lamellar-type pattern, Cells from cortisol-producing adenomas showed large round mitochondria with vesicular or tubulovesicular inner membranes surrounded by a characteristic dilated smooth endoplasmic reticulum, A highly unusual progesterone-producing adenoma, in which a deficiency of 21 alpha-hydroxylase activity was demonstrated, showed a peculiar type of enlarged lamellar mitochondria with bright inner matrix and a reduced number of inner membranes. Therefore, the ultrastructural characteristics of adrenal cortical mitochondria appear to be potential markers for the differentiation of steroid-producing adenomas, These studies point to the possibility of a broader use of electron microscopy in the study of adrenal tumors. C1 UNIV MIAMI,SCH MED,DEPT MED,MIAMI,FL. US DEPT VET AFFAIRS,MED CTR,MIAMI,FL. RP Bornstein, SR (reprint author), UNIV LEIPZIG,ZENTRUM INNERE MED,MED KLIN POLIKLIN 3,DEPT INTERNAL MED 3,PH ROSENTHAL STR 27,D-04103 LEIPZIG,GERMANY. NR 24 TC 9 Z9 10 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0018-5043 J9 HORM METAB RES JI Horm. Metab. Res. PD APR PY 1996 VL 28 IS 4 BP 177 EP 182 DI 10.1055/s-2007-979155 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UF892 UT WOS:A1996UF89200004 PM 8740192 ER PT J AU Xu, Y Davidson, L Alt, FW Baltimore, D AF Xu, Y Davidson, L Alt, FW Baltimore, D TI Deletion of the Ig kappa light chain intronic enhancer/matrix attachment region impairs but does not abolish V kappa J kappa rearrangement SO IMMUNITY LA English DT Article ID IMMUNOGLOBULIN GENE REARRANGEMENTS; PRE-B-CELLS; ALLELIC EXCLUSION; V(D)J RECOMBINATION; PROTEIN-BINDING; HEAVY; EXPRESSION; MU; TRANSCRIPTION; LINE AB Roles of the kappa intronic enhancer (iE kappa) and its asssociated matrix attachment region (MAR) during B cell development were examined using mutant embryonic stem (ES) cell lines in which the entire region on both chromosomes was replaced with either a recombined LoxP site (E kappa ND) or the PGK-neomycin resistance (PGK-neo(r)) gene (E kappa NI). B cells derived from E kappa ND ES cells had greatly impaired V kappa J kappa rearrangement, normal levels of kappa expression, and kappa:lambda ratios of 1:1 instead of the usual 10:1. Furthermore, lambda-producing hybridomas derived from E kappa ND cells displayed little kappa rearrangement. Thus, the MAR and iE kappa are quantitatively significant for kappa rearrangement but not necessary. In addition, little V kappa J kappa rearrangement could be detected in B cells derived from E kappa NI ES cells, demonstrating that an inserted PGK-neo(r) gene dominantly suppresses V kappa J kappa rearrangement. C1 CHILDRENS HOSP,HOWARD HUGHES MED INST,DEPT GENET & PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RP Xu, Y (reprint author), MIT,DEPT BIOL,77 MASSACHUSETTS AVE,CAMBRIDGE,MA 02139, USA. FU NIAID NIH HHS [AI-20047] NR 54 TC 139 Z9 139 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 1074-7613 J9 IMMUNITY JI Immunity PD APR PY 1996 VL 4 IS 4 BP 377 EP 385 DI 10.1016/S1074-7613(00)80251-4 PG 9 WC Immunology SC Immunology GA UH522 UT WOS:A1996UH52200006 PM 8612132 ER PT J AU Qu, XD Harwig, SSL Oren, A Shafer, WM Lehrer, RI AF Qu, XD Harwig, SSL Oren, A Shafer, WM Lehrer, RI TI Susceptibility of Neisseria gonorrhoeae to protegrins SO INFECTION AND IMMUNITY LA English DT Article ID ANTIMICROBIAL PEPTIDES; CATHEPSIN-G; GRANULOCYTES; GONOCOCCI AB We developed a sensitive and quantitative radial diffusion method to ascertain the susceptibility of six strains of Neisseria gonorrhoeae to antimicrobial peptides derived from mammalian leukocytes. The test organisms included the well-characterized serum-resistant FA19 and serum-sensitive F62 strains plus four antibiotic-resistant clinical isolates. Although each N. gonorrhoeae strain was resistant to human neutrophil defensins, all six were exquisitely sensitive to protegrins, a family of small beta-sheet antimicrobial peptides recently identified in porcine leukocytes. Protegrin-treated N. gonorrhoeae became vacuolated and had striking membrane changes when viewed by transmission and scanning electron microscopy. Because low concentrations of protegrins can also inactivate Chlamydia trachomatis and human immunodeficiency virus, they show promise for development as topical agents to avert sexually transmitted diseases. C1 UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT MED,LOS ANGELES,CA 90095. W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. EMORY UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,ATLANTA,GA 30322. VET ADM MED CTR,RES SERV,LABS MICROBIAL PATHOGENESIS,ATLANTA,GA 30033. FU NIAID NIH HHS [AI-22839, AI-37945, AI-21150] NR 19 TC 70 Z9 72 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1996 VL 64 IS 4 BP 1240 EP 1245 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA UC314 UT WOS:A1996UC31400023 PM 8606085 ER PT J AU Kaden, DA Warren, J Ryan, L Boorman, G Mellick, P AF Kaden, DA Warren, J Ryan, L Boorman, G Mellick, P TI The NTP/HEI collaborative ozone project on the health effects of chronic ozone inhalation SO INHALATION TOXICOLOGY LA English DT Article ID COLLAGEN-METABOLISM; AMBIENT LEVELS; LUNG COLLAGEN; ADULT-RATS; PPM OZONE; EXPOSURE; BRONCHIOLITIS; CONSEQUENCES; EPITHELIUM; RESPONSES AB Although many people are exposed to ozone, the effects of chronic exposure to this ubiquitous pollutant, especially low-level chronic exposure, are not well understood. The U.S. Environmental Protection Agency (EPA) current national ambient air quality standard for ozone is exceeded in many communities, especially during the summer. The standard is attained when the number of days per calendar year with maximum hourly average concentrations above 0.12 ppm is equal to or less than 1. The U.S. EPA estimates that 67 million people in the United States, or slightly more than a quarter of the residents, live in areas that were out of compliance with the current National Ambient Air Quality Standard (NAAQS) for ozone in 1989. Although there have been some studies of long-term exposure to ozone, many important questions remain about the health effects of chronic ozone exposure. The Health Effects Institute (HEI), in conjunction with the National Toxicology Program (NTP) carcinogenesis studies, has completed a major effort to help answer these questions. NTP included additional animals in its study for HEI investigators. Included in this effort is a set of studies examining histopathological, biochemical, morphological, and functional alterations in rats exposed to 0, 0.12, 0.5 or 1.0 ppm ozone for 20 mo. This article describes several aspects of this effort. This project can serve as a model for other large toxicological studies for which cancer may not be the only endpoint of concern. The additional animals required for the NTP/HEI Collaborative Ozone Project only represented a modest incremental cost, yet provided information on a much broader range of potential effects of ozone than the basic NTP carcinogenesis studies. C1 HARVARD UNIV, SCH PUBL HLTH, DANA FARBER CANC INST, BOSTON, MA 02115 USA. NIEHS, RES TRIANGLE PK, NC 27709 USA. PACIFIC NW LAB, RICHLAND, WA 99352 USA. RP Kaden, DA (reprint author), HLTH EFFECTS INST, 141 PORTLAND ST, SUITE 7300, CAMBRIDGE, MA 02139 USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 NR 47 TC 1 Z9 1 U1 0 U2 0 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0895-8378 J9 INHAL TOXICOL JI Inhal. Toxicol. PD APR PY 1996 VL 8 IS 3 BP 213 EP 227 DI 10.3109/08958379609005431 PG 15 WC Toxicology SC Toxicology GA UJ171 UT WOS:A1996UJ17100001 ER PT J AU Catalano, PJ Ryan, LM Kaden, DA AF Catalano, PJ Ryan, LM Kaden, DA TI Statistical design aspects of the NTP/HEI collaborative study on the health effects of chronic ozone inhalation SO INHALATION TOXICOLOGY LA English DT Article ID LONGITUDINAL DATA-ANALYSIS; CONTINUOUS OUTCOMES; MULTIPLE ENDPOINTS; DISCRETE; MODELS AB The purpose of the NTP/HEI Collaborative Study was to assess exposure- and concentration-related health effects associated with chronic exposure to ozone. Data were obtained from 164 animals specially dedicated to HEI from a standard ozone inhalation study conducted by Battelle Pacific Northwest Laboratories for the National Toxicology Program. The study involved a number of investigators, each interested in assessing a different type of ozone-related health effect, including respiratory function, as well as structural, cellular and biochemical changes in the nose, lungs, and airways. Designing and analyzing a study with multiple investigators raises many statistical challenges. The highest design priority was that each investigator's data be individually interpretable as an independent study. This means that each investigator had to be assigned an adequate number of animals, balanced with respect to concentration level and other factors such as gender and time of sacrifice. An additional feature of the collaborative study was the opportunity it provided to assess and quantify the effect of ozone exposure on a broad spectrum of outcomes, and to explore the relationship between the different types of effect. For example, the data allowed an assessment of whether the animals with the greatest degree of structural damage were also the ones with altered biochemistry. Maximizing the potential to assess these types of correlations required that investigators overlap as much as possible on measurements in individual animals. This aspect of the statistical design requires careful consideration of the compatibility between various investigators. Fortunately, the degree of compatibility was high. In most cases, for example, it was possible to assess respiratory function in the animals prior to their sacrifice, and then to divide the tissue between several different investigators. This article focuses on the statistical design of the collaborative project. Brief descriptions of each component investigation are given along with a discussion of logistical and other practical constraints. The allocation design of matching investigator groups to animal blocks is then presented, followed by a discussion of the impact of sample loss. The article concludes with a discussion of the features of the design that could be applied to future studies. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HLTH EFFECTS INST,CAMBRIDGE,MA. RP Catalano, PJ (reprint author), DANA FARBER CANC INST,DIV BIOSTAT,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 NR 12 TC 2 Z9 2 U1 0 U2 0 PU TAYLOR & FRANCIS PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0895-8378 J9 INHAL TOXICOL JI Inhal. Toxicol. PD APR PY 1996 VL 8 IS 3 BP 229 EP 249 DI 10.3109/08958379609005432 PG 21 WC Toxicology SC Toxicology GA UJ171 UT WOS:A1996UJ17100002 ER PT J AU Orr, SP Shalev, AY Rauch, SL Pitman, RK AF Orr, SP Shalev, AY Rauch, SL Pitman, RK TI Automatic psychophysiology of post-traumatic stress disorder SO INTEGRATIVE PHYSIOLOGICAL AND BEHAVIORAL SCIENCE LA English DT Meeting Abstract C1 VET ADM MED CTR,MANCHESTER,NH. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. HADASSAH UNIV HOSP,IL-91120 JERUSALEM,ISRAEL. NR 0 TC 0 Z9 0 U1 0 U2 1 PU TRANSACTION PERIOD CONSORTIUM PI NEW BRUNSWICK PA DEPT 3091 RUTGERS-THE STATE UNIV OF NJ, NEW BRUNSWICK, NJ 08903 SN 1053-881X J9 INTEGR PHYS BEH SCI JI Integr. Physiol. Behav. Sci. PD APR-JUN PY 1996 VL 31 IS 2 BP 183 EP 184 PG 2 WC Psychology, Biological; Neurosciences SC Psychology; Neurosciences & Neurology GA UT652 UT WOS:A1996UT65200038 ER PT J AU Alonso, A Rutan, JS AF Alonso, A Rutan, JS TI Separation and individuation in the group leader SO INTERNATIONAL JOURNAL OF GROUP PSYCHOTHERAPY LA English DT Article AB Psychodynamic group therapy, by definition, offers group members an opportunity to revisit some of the earliest developmental stages. The authors argue that conflicts around separation and individuation are stimulated with each beginning and ending of an intimate group. The leader of that group is similarly challenged around these primary conflicts. The question of group contagion, difficulties around the capacity to be alone, and the problems of projective identification are explored as they have an impact on leaders in a group. Case examples are offered to illustrate leadership problems along these dimensions. C1 MASSACHUSETTS GEN HOSP,CTR PSYCHOANALYT STUDIES,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,CTR GRP PSYCHOTHERAPY,BOSTON,MA 02114. NR 36 TC 7 Z9 7 U1 0 U2 2 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0020-7284 J9 INT J GROUP PSYCHOTH JI Int. J. Group Psychother. PD APR PY 1996 VL 46 IS 2 BP 149 EP 162 PG 14 WC Psychology, Clinical SC Psychology GA UE739 UT WOS:A1996UE73900001 PM 8935759 ER PT J AU Gans, JS AF Gans, JS TI The leader's use of indirect communication in group therapy SO INTERNATIONAL JOURNAL OF GROUP PSYCHOTHERAPY LA English DT Article ID GROUP-PSYCHOTHERAPY AB Indirect Communication (IC) is a leadership technique designed for those situations in which the leader must respond immediately but doing so directly might be a clinical mistake. As defined in this report IC refers to times when the leader addresses someone by speaking about that person to someone else or by thinking aloud while speaking to no one in particular The author distinguishes IC from other modes of indirect communication. Pitfalls of direct communication and ways in which IC avoids them and provides therapeutic alternatives are discussed. The leader's use of IC helps achieve two major goals: (1) the creation of an enlarged work space, safe enough for patients to express their more irrational and distressing feelings, and (2) the therapeutic handling of these uncivilized parts of each member as they emerge. Several clinical examples are presented. Misuses of IC are discussed. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. NR 19 TC 11 Z9 11 U1 1 U2 1 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0020-7284 J9 INT J GROUP PSYCHOTH JI Int. J. Group Psychother. PD APR PY 1996 VL 46 IS 2 BP 209 EP 228 PG 20 WC Psychology, Clinical SC Psychology GA UE739 UT WOS:A1996UE73900005 PM 8935763 ER PT J AU Young, RH AF Young, RH TI Introduction to new series on historical aspects of gynecologic pathology: Its personalities and literature SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Editorial Material RP Young, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD APR PY 1996 VL 15 IS 2 BP 93 EP 93 DI 10.1097/00004347-199604000-00001 PG 1 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA UE290 UT WOS:A1996UE29000001 ER PT J AU Eichhorn, JH Young, RH Clement, PB AF Eichhorn, JH Young, RH Clement, PB TI Sertoliform endometrial adenocarcinoma: A study of four cases SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE endometrium; sertoliform adenocarcinoma; uterine tumor resembling ovarian sex-cord tumor; endometrial stromal sarcoma; sex-cord-like elements ID CORD STROMAL TUMORS; CARCINOMAS; NEOPLASMS; UTERUS; DIFFERENTIATION; SARCOMAS AB We studied four endometrial carcinomas with a conspicuous component that resembled patterns in Sertoli cell tumors. The patients presented at age 44-83 years (mean 65 years), with abnormal or postmenopausal vaginal bleeding in three and abnormal cervical cytology in one. All were multiparous, moderately to markedly obese, and hypertensive, and three patients had non-insulin-dependent diabetes mellitus. One tumor was suspected to be an endometrial stromal sarcoma with sex-cord-like differentiation on biopsy. Gross examination of the hysterectomy and bilateral salpingo-oophorectomy specimens showed solid polypoid endometrial tumors in each case, Light microscopic examination showed three to be superficially invasive of the myometrium and one to be confined to the endometrium; none of the tumors showed the tonguelike pattern of myoinvasion or the angiolymphatic invasion characteristic of low-grade endometrial stromal sarcomas. The sertoliform component, which predominated in one case and was only focal in the three others, was composed of uniform small hollow tubules lined by columnar cells with apical cytoplasm and of compact slender cords. The tubules and cords were often present between benign-appearing or carcinomatous glands. In the case with predominant sertoliform areas, the lesional cells had clear cytoplasm suggesting a lipid-rich variant; special stains of this case demonstrated cytoplasmic glycogen but no fat. In none of the cases was cytoplasmic mucin, argyrophil granules, or argentaffinity demonstrated. The nonsertoliform areas of the tumors consisted of typical endometrioid adenocarcinoma; concurrent endometrial hyperplasia was also present in each case. Squamous differentiation and minor foci of anaplastic carcinoma with bizarre tumor giant cells were present in three tumors. Immunoperoxidase stains showed staining for two or more markers of epithelial or glandular differentiation in the sertoliform areas in all cases (keratin, epithelial membrane antigen, carcinoembryonic antigen, CA125, TAG72), with focal expression of vimentin in all cases. In none of the cases was desmin or actin staining observed. The evidence indicates that tumors in this series are variants of endometrioid adenocarcinoma and are distinct from uterine tumors resembling ovarian sex-cord tumors and stromal sarcomas with sex-cord-like differentiation. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA. VANCOUVER HOSP & HLTH SCI CTR,DEPT PATHOL,VANCOUVER,BC,CANADA. UNIV BRITISH COLUMBIA,DEPT PATHOL,VANCOUVER,BC,CANADA. RP Eichhorn, JH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,WARREN 120,BOSTON,MA 02114, USA. NR 18 TC 19 Z9 21 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD APR PY 1996 VL 15 IS 2 BP 119 EP 126 DI 10.1097/00004347-199604000-00005 PG 8 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA UE290 UT WOS:A1996UE29000005 PM 8786200 ER PT J AU Maxwell, M Galanopoulos, T NevilleGolden, J Antoniades, HN AF Maxwell, M Galanopoulos, T NevilleGolden, J Antoniades, HN TI Overexpression of the ros1 gene in primary human gliomas may contribute to malignant progression SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE glioma; ros1; cell-cycle; tumorigenesis ID PRIMARY HUMAN ASTROCYTOMAS; MESSENGER-RNAS; CELL-LINES; EXPRESSION; GROWTH; SEQUENCE; CDNA; AMPLIFICATION; ANGIOGENESIS; CONSERVATION AB Gliomas are malignant brain tumors thought to arise through multi-step tumorigenesis, involving both the activation of oncogenes and the loss of tumor suppressor genes. The ros1 gene encodes a proto-oncogenic protein which has been implicated, by in vitro studies, in the pathogenesis of several types of cancer, including gliomas. Northern blot analysis revealed expression of ros1 mRNA in 3 (30%) of 10 primary glioma specimens. In situ hybridization localized ros1 mRNA transcripts to GFAP positive tumor cells and pericytes around capillaries. Immunohistochemistry using an antibody specific for ros1 demonstrated strong positivity amongst neoplastic glial cells in the same glioma samples. No ros1 mRNA or protein was detected in 5 normal brain specimens. These data provide the first evidence for the overexpression of ros1 mRNA and protein in primary human gliomas, and are consistent with a proposed oncogenic role of ros1 in these tumors. C1 HARVARD UNIV,SCH MED,BOSTON,MA. HARVARD UNIV,SCH PUBL HLTH,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. UNIV OXFORD,RADCLIFFE INFIRM,DEPT NEUROPATHOL,OXFORD OX2 6HE,ENGLAND. RP Maxwell, M (reprint author), MASSACHUSETTS GEN HOSP,NEUROSURG SERV,HOUSE MAIL,FRUIT ST,BOSTON,MA 02114, USA. NR 32 TC 1 Z9 1 U1 0 U2 0 PU PROFESSOR D A SPANDIDOS PI ATHENS PA 1, S MERKOURI ST, EDITORIAL OFFICE,, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD APR PY 1996 VL 8 IS 4 BP 713 EP 718 PG 6 WC Oncology SC Oncology GA UB251 UT WOS:A1996UB25100011 PM 21544418 ER PT J AU Gerweck, LE Zaidi, ST AF Gerweck, LE Zaidi, ST TI The reproducibility and relationship between single and fractionated dose estimates of the surviving fraction at 2 Gy SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE radiosensitivity; reproducibility; predictive assays; fractionated irradiation ID HUMAN-MELANOMA XENOGRAFTS; LOCAL TUMOR-CONTROL; SQUAMOUS-CELL CARCINOMAS; HUMAN-MALIGNANT GLIOMAS; RADIATION SENSITIVITY; INVITRO RADIOSENSITIVITY; INVIVO RADIORESPONSE; IRRADIATION; RADIOTHERAPY; HETEROGENEITY AB Purpose: To evaluate the reproducibility and relationship between the surviving fraction at 2 Gy obtained from single-graded dose and multifraction survival curve assays, Methods and Materials: Single-graded dose and multifraction survival curve assays were concurrently performed in five human cell lines, For the multifraction studies, five to six doses at 2 Gy per fraction were administered with a time interval of 5.5 h between fractions. All surviving fraction data was corrected for multiplicity and cell proliferation during treatment, Replicate experiments were performed for each cell line. Results: The precision of the Sf2 estimates obtained from multifraction studies was approximately three times greater than was obtained in the single-dose studies. For the single-dose studies, the average difference between the Sf2s obtained in the initial vs, repeat experiment was 0.11; for the fractionated-dose studies the difference was significantly reduced to 0.032. A rank-order correlation was not obtained between the 2 Gy Sfs in the initial and repeat single-dose assays; in the multifraction studies, the correlation was significant (p < 0.05). The rank-order correlation between the single- and fractionated-dose Sf2 assays was significant only when the two sets of assays were pooled; however, the coefficient of correlation remained low (R(2) = 0.50). Conclusions: The precision of the estimates of the surviving fraction at 2 Gy, obtained from multifraction assays, was substantially greater than was obtained in single dose-survival curve assays. RP Gerweck, LE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA22860] NR 26 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD APR 1 PY 1996 VL 35 IS 1 BP 81 EP 87 DI 10.1016/S0360-3016(96)85014-0 PG 7 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA UG528 UT WOS:A1996UG52800010 PM 8641930 ER PT J AU Galvin, JM Leavitt, DD Smith, AA AF Galvin, JM Leavitt, DD Smith, AA TI Field edge smoothing for multileaf collimators SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE multileaf; penumbra AB Purpose: To smooth the scalloped dose pattern that occurs for stepped leaves at a treatment field edge defined by a multileaf collimator. Methods and Materials: Fields with centers shifted slightly in space were superimposed to blur the staggered dose distribution at the field edge, Film dosimetry was used to monitor changes, The dose distribution for a single field position was compared to the distribution for one and three shifts, Three depths were examined and divergent alloy blocks were included in the comparison, Results: The structure that appears at an edge for a single field when leaves are staggered was nearly eliminated when the field was shifted three times to give a total of four different positions, However, shifting the held one time so that two fields were superimposed gave an intermediate result with only slight improvement in the undulating dose distribution, For the four superimposed fields, the 50% isodose pattern converged to a smoothed line running along the center of the original undulating pattern, The 80 and 20% isodoses did not converge to the center of their scalloped patterns, Instead, these isodose lines were spread leaving a larger penumbra width than a divergent alloy block, Conclusions: Shifting and adding fields is an effective method for smoothing the staggered dose distribution that results when the leaves of a multileaf collimator are stepped to form an irregular field pattern. However, the width of the penumbra for the combined fields is wider than the penumbra for a cerrobend block. C1 NYU,MED CTR,DEPT RADIOL,NEW YORK,NY 10016. UNIV UTAH,SCH MED,DEPT RADIOL,SALT LAKE CITY,UT 84132. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,BOSTON,MA. NR 8 TC 25 Z9 26 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD APR 1 PY 1996 VL 35 IS 1 BP 89 EP 94 DI 10.1016/S0360-3016(96)85015-2 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA UG528 UT WOS:A1996UG52800011 PM 8641931 ER PT J AU Bursell, SE Clermont, AC Kinsley, BT Simonson, DC Aiello, LM Wolpert, HA AF Bursell, SE Clermont, AC Kinsley, BT Simonson, DC Aiello, LM Wolpert, HA TI Retinal blood flow changes in patients with insulin-dependent diabetes mellitus and no diabetic retinopathy - A video fluorescein angiography study SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE diabetes; fluorescein angiography; glucose clamp; hyperglycemia; retina; retinal blood flow ID LASER DOPPLER VELOCIMETRY; MEAN CIRCULATION TIME; FLUOROPHOTOMETRY; HYPERGLYCEMIA; GLUCOSE; PLASMA AB Purpose. The authors investigated retinal blood flow changes in patients with insulin-dependent diabetes mellitus (IDDM) and no diabetic retinopathy compared to age-matched subjects without diabetes. They also investigated whether blood glucose levels could modulate retinal blood flow in these patients with diabetes and whether this modulation would impact retinal blood flow data used in cross-sectional studies assessing changes in retinal blood flow. Methods, Retinal blood flow was measured using video fluorescein angiography, and blood glucose levels were manipulated using glucose clamp methodologies with continuous basal insulin replacement. Blood glucose levels were clamped at 100, 200, and 300 mg/dl. Retinal blood flow measurements were performed at each blood glucose level after subjects had been stabilized for an hour at each of the different blood glucose levels. Results. Retinal blood flow was found to be significantly decreased (P < 0.01) in the group of patients with no diabetic retinopathy (19.4 +/- 4.6 arbitrary units [AU]) compared to retinal blood flow in subjects without diabetes (28.7 +/- 6.4 AU). During glucose clamp adjustment of blood glucose levels, it was found that as blood glucose levels were increased from euglycemia (100 mg/dl) to 200 mg/dl and to 300 mg/dl, retinal blood flow was significantly increased at the 200 mg/dl level (21.5 +/- 4.7 AU, P < 0.05) and at the 300 md/dl level (25.9 +/- 8.8 AU, P < 0.01) compared to the 100 mg/dl level (16.3 +/- 3.8 AU). In addition, the retinal blood flow at the 100 and 200 mg/dl levels was significantly reduced (P < 0.01) compared to nondiabetic retinal blood flow (28.7 +/- 6.4 AU). Conclusions. Retinal blood flow was found to be decreased in patients with IDDM with no diabetic retinopathy, and acute elevations in blood glucose levels resulted in increased retinal blood flow in these patients. The acute modulation of retinal blood flow by blood glucose levels should be considered in cross-sectional studies investigating retinal blood flow changes in patients with diabetes. The results from this study indicate that if blood glucose levels are not accounted for in the analyses, larger populations would have to be studied to demonstrate statistically significant differences between groups with and without diabetes. C1 JOSLIN DIABET CTR,DEPT INTERNAL MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA. RP Bursell, SE (reprint author), JOSLIN DIABET CTR,BEETHAM EYE INST,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NEI NIH HHS [EY09062] NR 39 TC 192 Z9 202 U1 0 U2 5 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD APR PY 1996 VL 37 IS 5 BP 886 EP 897 PG 12 WC Ophthalmology SC Ophthalmology GA UD853 UT WOS:A1996UD85300020 PM 8603873 ER PT J AU Sandberg, MA Pawlyk, BS Berson, EL AF Sandberg, MA Pawlyk, BS Berson, EL TI Isolation of focal rod electroretinograms from the dark-adapted human eye SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE electroretinography; focal; multiple evanescent white dot syndrome (MEWDS); retina; rod ID RETINITIS-PIGMENTOSA; CONE ELECTRORETINOGRAMS; DEGENERATION AB Purpose, To isolate focal rod electroretinograms (ERGs) from the dark-adapted human eye. Methods, In two normal volunteers, dark-adapted focal rod ERGs were recorded from the peripheral retina in response to 30 degrees diameter blue flashes of varying retinal illuminance and from different retinal regions in response to 10 degrees diameter bright blue flashes. Dark-adapted focal rod ERGs also were recorded from a patient with the multiple evanescent white dot syndrome (MEWDS) and an enlarged blind spot in response to 30 degrees diameter blue flashes presented within and outside the scotoma. The slower and larger stray light rod component elicited by these flashes was removed by subtracting the matching rod response to a dimmer, full-field flash, or was ignored when it did not overlap the faster and smaller focal rod component. Results. The focal rod ERG had a waveform and sensitivity similar to those of the full-field rod ERG, was approximately proportional in amplitude to the density of rods directly illuminated, and was nondetectable within the retinal area corresponding to the enlarged blind spot of the patient with MEWDS. Conclusions, Focal rod ERG a- and b-waves, in response to stimuli as small as 10 degrees, can be recorded from different regions of the dark-adapted human retina to evaluate localized rod function. RP Sandberg, MA (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY00169, EY08398] NR 20 TC 8 Z9 8 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD APR PY 1996 VL 37 IS 5 BP 930 EP 934 PG 5 WC Ophthalmology SC Ophthalmology GA UD853 UT WOS:A1996UD85300025 PM 8603878 ER PT J AU Harris, WH AF Harris, WH TI Modularity is unnecessary in primary femoral THA but has some advantages in primary acetabular THA SO JOURNAL OF ARTHROPLASTY LA English DT Editorial Material RP Harris, WH (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,DEPT ORTHOPAED SURG,GRJ 1126,32 FRUIT ST,BOSTON,MA 02114, USA. NR 2 TC 3 Z9 3 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0883-5403 J9 J ARTHROPLASTY JI J. Arthroplast. PD APR PY 1996 VL 11 IS 3 BP 334 EP 336 DI 10.1016/S0883-5403(96)80087-8 PG 3 WC Orthopedics SC Orthopedics GA UF861 UT WOS:A1996UF86100016 PM 8713915 ER PT J AU Bauman, ML AF Bauman, ML TI Brief report: Neuroanatomic observations of the brain in pervasive developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Working Conference on the State of the Science in Autism CY APR, 1995 CL NIH, WASHINGTON, D.C. HO NIH ID INVOLVEMENT; HIPPOCAMPUS; AMYGDALA; CATS RP Bauman, ML (reprint author), MASSACHUSETTS GEN HOSP, DEPT NEUROL, 32 FRUIT ST, BURNHAM 731, BOSTON, MA 02115 USA. NR 18 TC 54 Z9 54 U1 0 U2 0 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD APR PY 1996 VL 26 IS 2 BP 199 EP 203 DI 10.1007/BF02172012 PG 5 WC Psychology, Developmental SC Psychology GA UH449 UT WOS:A1996UH44900013 PM 8744485 ER PT J AU Mitlak, BH BurdetteMiller, P Schoenfeld, D Neer, RM AF Mitlak, BH BurdetteMiller, P Schoenfeld, D Neer, RM TI Sequential effects of chronic human PTH (1-84) treatment of estrogen-deficiency osteopenia in the rat SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID PARATHYROID-HORMONE 1-34; OSTEOPOROTIC PATIENTS; BONE MASS; OVARIECTOMIZED RATS; TRABECULAR BONE; CORTICAL BONE; SPINAL BONE; INCREASE; 1,25-DIHYDROXYVITAMIN-D; INTERMITTENT AB Although daily injections of parathyroid hormone (PTH) can rapidly reverse estrogen-deficiency bone loss in rats, PTH treatment of osteoporotic humans has to date produced more modest increases in bone mass, To explore the reasons for this important difference, we evaluated the dose- and time-dependence of human PTH 1-84 treatment effects on bone mass and biochemical markers of bone metabolism in rats with estrogen-deficiency bone loss, The highest doses of PTH increased spinal, femoral, and total skeletal mass to supra-normal levels and stimulated cortical endosteal bone formation, Spine and whole skeleton mass and density increased rapidly at first, but then increased more slowly; the rate of change decreased significantly (p < 0.01) during continued treatment with the highest doses of PTH, The effects of PTH treatment on biochemical markers also were both dose-dependent and time-dependent, Serum osteocalcin, a marker of osteoblast function, increased with the highest doses of PTH (p < 0.001), but reached an early plateau and later returned toward baseline, Urinary excretion of pyridinolines, a marker of osteoclast function, increased in a time-dependent fashion throughout treatment (p < 0.001), Serum 1,25(OH)(2) vitamin D levels increased in a dose-related fashion, but then decreased toward control levels despite continued treatment. We demonstrate that both osteoblast and osteoclast function are increased during daily PTH therapy in the rat, The pattern of response depends on both the dose of PTH and the duration of therapy, These dose- and time-related effects should be taken into account when designing experimental PTH treatments for osteoporosis, and they deserve intensive study. RP Mitlak, BH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,SCH MED,DEPT MED,BUL-327,BOSTON,MA 02114, USA. NR 41 TC 39 Z9 39 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD APR PY 1996 VL 11 IS 4 BP 430 EP 439 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UC130 UT WOS:A1996UC13000002 PM 8992873 ER PT J AU Berger, JW Talamo, JH LaMarche, KJ Kim, SH Snyder, RW DAmico, DJ Marcellino, G AF Berger, JW Talamo, JH LaMarche, KJ Kim, SH Snyder, RW DAmico, DJ Marcellino, G TI Temperature measurements during phacoemulsification and erbium:YAG laser phacoablation in model systems SO JOURNAL OF CATARACT AND REFRACTIVE SURGERY LA English DT Article ID ER-YAG; PULSE DURATION; THERMAL-DAMAGE; TISSUE-TYPE; ABLATION; PHACOLYSIS; YSGG; LENS AB Purpose: To compare the potential for thermal injury to ocular structures resulting from phacoemulsification ultrasound energy and erbium,YAG (Er:YAG) laser output. Setting: Morse Laser Laboratory, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston. Methods: Ultrasonic phacoemulsification energy and Er:YAG laser output (10 J/cm(2), 10 Hz, 0.3 watts) sufficient for lens removal were applied to model systems and human cadaver eyes. Temperatures were measured with ultrafine thermocouples interfaced to a microcomputer data acquisition system. Results: Although greater than 95% of energy from laser output is converted to thermal energy, temperature rise in model systems and cadaver eyes was 10 to 15 times greater after pulsed application of ultrasound energy than after Er:YAG laser application. At 100% power, similar to 4 watts of ultrasound power is converted to heat. Temperature rise following both laser and ultrasound applications decreased with irrigation in cadaver eyes and increasing volume in a model system. With continuous irrigation (20 cc/min), the temperature rise at 2 minutes measured al the corneal endothelial surface, within the corneal stroma, and in the anterior chamber angle of cadaver eyes was similar to 0.5 degrees Celsius (degrees C) after laser application and 7.0 degrees C after ultrasound application. Without irrigation, temperatures rose 2.5 degrees C after laser application and 35.0 degrees C after ultrasound application. Conclusion: At operating parameters sufficient for lens removal, the Er:YAG laser imparted less thermal energy to whole eyes and model systems than ultrasonic phacoemulsification. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,LASER RES LAB,BOSTON,MA 02114. NR 24 TC 26 Z9 29 U1 0 U2 0 PU AMER SOC CATARACT REFRACTIVE SURGERY PI FAIRFAX PA 4000 LEGATO RD, SUITE 850, FAIRFAX, VA 22030 SN 0886-3350 J9 J CATARACT REFR SURG JI J. Cataract. Refract. Surg. PD APR PY 1996 VL 22 IS 3 BP 372 EP 378 PG 7 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA UE697 UT WOS:A1996UE69700028 PM 8778374 ER PT J AU Kasinath, BS Grellier, P Choudhury, GG Abboud, SL AF Kasinath, BS Grellier, P Choudhury, GG Abboud, SL TI Regulation of basement membrane heparan sulfate proteoglycan, perlecan, gene expression in glomerular epithelial cells by high glucose medium SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID CARBOHYDRATE RESPONSE ELEMENT; HELIX ZIPPER PROTEIN; DIABETIC NEPHROPATHY; DNA-BINDING; IDENTIFICATION; COMPONENTS; ANTIBODIES; PRECURSOR; RATS; MYC AB Proteinuria in diabetic nephropathy has been correlated with reduction in heparan sulfate proteoglycan (HSPG) content of the glomerular basement membrane. We have previously shown that the underlying mechanism probably involves reduction in the synthesis by glomerular epithelial cells. In this study we explored whether high glucose medium regulates basement membrane HSPG gene expression. Northern analysis demonstrated that rat glomerular epithelial cells in vitro constitutively express mRNA for basement membrane HSPG, similar to that observed in rat kidney glomerulus. RNase protection assay showed that incubation of glomerular epithelial cells with 30 mM glucose for 24 h and 7 days resulted in reduction in HSPG mRNA abundance. The decrease in mRNA abundance correlated with reduction in the synthesis of (SO4)-S-35-labeled basement membrane HSPG as measured by immunoprecipitation. Reduction in synthesis of HSPG could not be entirely accounted for by decrease in mRNA abundance, suggesting both transcriptional and posttranscriptional mechanisms may be involved in reduction of glomerular basement membrane HSPG synthesis by glomerular epithelial cells in diabetic nephropathy. (C) 1996 Wiley-Liss, Inc.** RP Kasinath, BS (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,AUDIE L MURPHY MEM VET ADM HOSP,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIAMS NIH HHS [AR42306]; NIDDK NIH HHS [DK41517] NR 36 TC 24 Z9 25 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD APR PY 1996 VL 167 IS 1 BP 131 EP 136 DI 10.1002/(SICI)1097-4652(199604)167:1<131::AID-JCP15>3.0.CO;2-E PG 6 WC Cell Biology; Physiology SC Cell Biology; Physiology GA UA977 UT WOS:A1996UA97700015 PM 8698830 ER PT J AU Horner, MD Flashman, LA Freides, D Epstein, CM Bakay, RAE AF Horner, MD Flashman, LA Freides, D Epstein, CM Bakay, RAE TI Temporal lobe epilepsy and performance on the Wisconsin Card Sorting Test SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Article AB The replicability of previous evidence for differential performance between left and right temporal lobe epileptic patients on the Wisconsin Card Sorting Test (WCST) was evaluated in a new sample of candidates for focal resection. Many subjects obtained high scores on indices of perseveration, which are commonly thought to reflect frontal dysfunction, but there were no differences in performance between patients with language-dominant and nondominant temporal foci. The findings confirm existing evidence that performance decrements on the WCST can be associated with epileptic foci and focal lesions in nonfrontal brain regions. C1 MED UNIV S CAROLINA,CHARLESTON,SC 29425. EMORY UNIV,ATLANTA,GA 30322. DARTMOUTH COLL SCH MED,LEBANON,NH. RP Horner, MD (reprint author), RALPH H JOHNSTON DVA MED CTR,PSYCHIAT SERV 116B,109 BEE ST,CHARLESTON,SC 29401, USA. NR 9 TC 30 Z9 30 U1 0 U2 0 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD APR PY 1996 VL 18 IS 2 BP 310 EP 313 DI 10.1080/01688639608408285 PG 4 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA UR524 UT WOS:A1996UR52400014 PM 8780965 ER PT J AU Wang, QF Khoury, RH Smith, PC McConnell, DS Padmanahban, V Midgley, AR Schneyer, AL Crowley, WF Sluss, PM AF Wang, QF Khoury, RH Smith, PC McConnell, DS Padmanahban, V Midgley, AR Schneyer, AL Crowley, WF Sluss, PM TI A two-site monoclonal antibody immunoradiometric assay for human follistatin: Secretion by a human ovarian teratocarcinoma-derived cell line (PA-1) SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID FOLLICLE-STIMULATING-HORMONE; ACTIVIN-BINDING PROTEIN; RIBONUCLEIC-ACID LEVELS; RAT GRANULOSA-CELLS; LUTEINIZING-HORMONE; ESTROUS-CYCLE; GROWTH-FACTOR; INHIBIN; EXPRESSION; PITUITARY AB The follistatin/activin/inhibin system increasingly appears to have important growth and differentiating effects in a variety of cell types, including cancer. We have developed a two-site immunoradiometric assay for measurement of human follistatin using two monoclonal antibodies against recombinant human follistatin. This cloned protein donor assay is sensitive (0.5 ng/mL), specific for free human follistatin, and precise (<5% within assay coefficient of variation). Using this assay, native human follistatin could be measured in human pituitary extracts, follicular fluid, and granulosa-luteal cell-conditioned medium. To identify and characterize human follistatin secreted by ovarian cancer cells, we screened five human ovarian carcinoma cell lines currently available from the American Type Culture Collection (Rockville, MD). One of these, a cell line derived from a teratocarcinoma (designated PA-1, American Type Culture Collection, CRL1572), secreted large (3 mu g/10(6) cells per 24 h) quantities of immunoreactive follistatin constituitively. Increasing volumes of conditioned medium from these cultured cells generated response curves parallel to those of recombinant human follistatin 288 reference protein, human follicular fluid, or culture medium from human granulosa-luteal cells. Secretion of follistatin by PA-1 cells was time and cell-number dependent with 297.9 +/- 15.2, 654 +/- 29.8, and 940 +/- 49.1 ng follistatin secreted over 24 h by 1 x 10(5), 2 x 10(5), and 3 x 10(5) cells, respectively. Western and ligand blot analysis revealed that the immunoreactive follistatin secreted by PA-1 cells and isolated by sulfate-cellufine chromatography was identical to the molecular weight variants (32,000 and 35,000 M(r)) of recombinant human follistatin 288. PA-1 cell-conditioned medium suppressed basal secretion of FSH by cultured rat anterior pituitary cells in a dose-dependent fashion. This follistatin bioactivity was completely removed by adsorption with either solid-phase monoclonal antifollistatin or a dextran-sulfate chromatography gel. Because activin suppressed the proliferation of PA-I cells, secretion of bioactive follistatin may represent an autocrine mechanism opposing activin to maintain the rapid growth rate of PA-1 cells. These observations demonstrate that the ovarian teratocarcinoma cell line, PA-1, secretes considerable amounts of human follistatin that is biologically active, capable of binding human activin, and antigenically similar to recombinant human follistatin 288. The monoclonal antibodies and two-site assay reported herein should be useful in assessing the regulation of follistatin secretion and as a dignostic tool, especially if follistatin measurements prove to be a marker for some ovarian cancers. C1 MASSACHUSETTS GEN HOSP, NATL COOPERAT PROGRAM INFERTIL RES, BOSTON, MA 02114 USA. UNIV MICHIGAN, ANN ARBOR, MI 48109 USA. FU NICHD NIH HHS [P30HD-28138, U54HD-29164, U54HD-29184] NR 51 TC 23 Z9 23 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1996 VL 81 IS 4 BP 1434 EP 1441 DI 10.1210/jc.81.4.1434 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UD666 UT WOS:A1996UD66600028 PM 8636347 ER PT J AU Sayegh, RA Tao, XJ Awwad, JT Isaacson, KB AF Sayegh, RA Tao, XJ Awwad, JT Isaacson, KB TI Localization of the expression of complement component 3 in the human endometrium by in situ hybridization SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID UTERINE EPITHELIUM INVITRO; LYMPHOID-CELLS; RAT UTERUS; SECRETION; ESTROGEN; ORGANIZATION; SEQUENCE; PROTEINS; TISSUE; C-3 AB C3 production by the human endometrium has been previously described. The objective of the current study was to localize the site of expression and regulation of the third component of complement, C3, in the endometrium. Eight secretory and eight proliferative archival endometrial samples from hysterectomy and endometrial biopsy specimens were used for in Situ hybridization analysis. This analysis was performed with a radiolabeled riboprobe synthesized from a 736-bp template representing sequence 1944-2680 of the human C3 complementary DNA. Duplicate sections were hybridized with sense and antisense riboprobes. Resultant autoradiograms were analyzed qualitatively by light- and darkfield microscopy. In proliferative endometrium, minimal expression of C3 was observed and was limited to a few stromal patches and glands throughout the section. In the secretory samples, prominent C3 expression was observed in both the glands and stroma of the basalis layer. Endometrial lymphocytes did not express C3. Endometrial stromal and glandular cells express the C3 gene. Endometrial lymphocytes did not express C3, but other nondistinct lymphoid elements scattered in the stroma may be expressing C3. There was a visibly more intense expression of C3 in the basalis layer of the secretory endometrium than in proliferative endometrium. The spatial and temporal pattern of C3 expression may have implications in normal menstrual physiology and in the immunological response of the endometrium to the invading trophoblast during placentation. RP Sayegh, RA (reprint author), HARVARD UNIV, VINCENT MEM OBSTET & GYNECOL SERV, MASSACHUSETTS GEN HOSP, SCH MED, BOSTON, MA 02114 USA. NR 23 TC 25 Z9 25 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1996 VL 81 IS 4 BP 1641 EP 1649 DI 10.1210/jc.81.4.1641 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UD666 UT WOS:A1996UD66600062 PM 8636381 ER PT J AU Sigal, RJ Doria, A Warram, JH Krolewski, AS AF Sigal, RJ Doria, A Warram, JH Krolewski, AS TI Codon 972 polymorphism in the insulin receptor substrate-1 gene, obesity, and risk of noninsulin-dependent diabetes mellitus SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article AB Because of the role of insulin receptor substrate-1 in insulin action, the insulin receptor substrate-1 gene is a candidate gene for noninsulin-dependent diabetes mellitus (NIDDM). Modest associations between NIDDM and a GGG-->AGG single base substitution (corresponding to a glycine-->arginine amino acid substitution) in codon 972 of the gene have been found, but none reached statistical significance. To examine further how large a proportion of NIDDM cases could be caused by the mutation, we performed a stratified analysis combining the results from the 6 earlier studies and those from our panel of 192 unrelated NIDDM subjects and 104 healthy controls. In addition, we looked for a possibility that the codon 972 mutation plays a role only in the presence of certain conditions. Genomic DNA samples obtained from NIDDM cases and healthy controls were genotyped using a PCR-restriction fragment length polymorphism protocol modified for genomic DNA. The GGG-->AGG substitution was found in 5.7% of the diabetic subjects (11 of 192) and 6.9% of the controls (7 of 104). The difference between groups was not statistically significant, and it was not different from the results of other studies. The Mantel-Haenszel summary odds ratio across all studies was 1.49 (P < 0.05; 95% confidence intervals, 1.01-2.2). This summary odds ratio is consistent with a small proportion of NIDDM cases (similar to 3%) being caused by the mutation. Exploratory subgroup analyses on our panel suggested a clustering of NIDDM, the codon 972 mutation, and overweight, raising the hypothesis that the mutation may predispose to NIDDM only in the presence of excess body weight. C1 JOSLIN DIABET CTR, DEPT EPIDEMIOL & GENET, SECT EPIDEMIOL & GENET, BOSTON, MA 02215 USA. FU NIDDK NIH HHS [P30-DK-36836] NR 9 TC 55 Z9 56 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1996 VL 81 IS 4 BP 1657 EP 1659 DI 10.1210/jc.81.4.1657 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UD666 UT WOS:A1996UD66600065 PM 8636384 ER PT J AU Meigs, JB Nathan, DM Cupples, LA Wilson, PWF Singer, DE AF Meigs, JB Nathan, DM Cupples, LA Wilson, PWF Singer, DE TI Tracking of glycated hemoglobin in the original cohort of the Framingham Heart Study SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE blood glucose; epidemiological factors; HBA(1C); hemoglobin A-glycosylated; longitudinal study ID DENSITY-LIPOPROTEIN CHOLESTEROL; DEPENDENT DIABETES-MELLITUS; GLYCOSYLATED HEMOGLOBIN; GLUCOSE-TOLERANCE; PLASMA-GLUCOSE; RETINOPATHY; POPULATION; ASSOCIATION; DISEASE; ASSAY AB Glycated hemoglobin measures average blood glucose over the preceding 2 to 3 months. The authors examined the tracking of the major glycated hemoglobin, hemoglobin A(1c) (HbA(1c)), over a period of 4 to 6 yeats. Two HbA(1c) measurements were obtained between 1986 and 1993 from 639 elderly, presumptively nondiabetic members of the original cohort of the Framingham Heart Study, Framingham, Massachusetts. Mean +/-C standard deviation (SD) baseline and follow-up HbA(1c) were 5.43% +/- 0.7 and 5.71% +/- 0.9, respectively. Intraclass correlation of 0.59 between baseline and follow-up measurements indicated good reliability of a single HbA(1c) measurement. Ninety-one percent of follow-up measurements were within +/- 20% of baseline value; HbA(1c) values tended to move 15% closer to the baseline mean over time. There was a modest tendency for HbA(1c) values to increase with time; the mean difference between measurements was 0.28% +/- 0.7 SD (P < 0.0001), Change in HbA(1c) was positively associated with age and body mass index at baseline examination, and negatively associated with cigarette smoking, even after controlling for age and body mass index. These effects were very small, however. We conclude that glycated hemoglobin reliably categorizes the glucose control of nondiabetic subjects over a period of 4 to 6 years, confirming its value as an epidemilogical measure. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,DIABET UNIT,BOSTON,MA 02114. BOSTON UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL & BIOSTAT,BOSTON,MA. BOSTON UNIV,SCH MED,BOSTON,MA 02118. FRAMINGHAM STUDY,FRAMINGHAM,MA. RP Meigs, JB (reprint author), MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,S50-3,BOSTON,MA 02114, USA. FU BHP HRSA HHS [2 T32 PE11001-06]; NHLBI NIH HHS [N01-HC-38038] NR 36 TC 59 Z9 59 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD APR PY 1996 VL 49 IS 4 BP 411 EP 417 DI 10.1016/0895-4356(95)00513-7 PG 7 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA UH716 UT WOS:A1996UH71600003 PM 8621991 ER PT J AU Rex, JH Pfaller, MA Lancaster, M Odds, FC Bolmstrom, A Rinaldi, MG AF Rex, JH Pfaller, MA Lancaster, M Odds, FC Bolmstrom, A Rinaldi, MG TI Quality control guidelines for National Committee for clinical laboratory standards-recommended broth macrodilution testing of ketoconazole and itraconazole SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID SUSCEPTIBILITY TESTS AB Ketoconazole and itraconazole were tested in a multilaboratory study to establish quality control (QC) guidelines for yeast antifungal susceptibility testing, Two isolates that had been previously identified as QC isolates for amphotericin B, fluconazole, and flucytosine (Candida parapsilosis ATCC 22019 and Candida krusei ATCC 6258) were tested in accordance with the National Committee for Clinical Laboratory Standards M27-P guidelines, Each isolate was tested 20 times with the two antifungal agents in the five laboratories by using a lot of RPMI 1640 unique to each laboratory as well as a lot common to all five laboratories, thus generating 200 MICs per drug per organism, Overall, 96 to 99% of the MICs for each drug fell within the desired 3-log(2) dilution range (mode +/- 1 log(2) dilution), By using these data, 3-log(2) dilution QC ranges encompassing 98% of the observed MICs for three of the organism-drug combinations and 94% of the observed MICs for the fourth combination were established, These QC ranges are 0.064 to 0.25 mu g/ml for both ketoconazole and itraconazole against C, parapsilosis ATCC 22019 and 0.125 to 0.5 mu g/ml for both ketoconazole and itraconazole against C. krusei ATCC 6258. C1 UNIV IOWA,COLL MED,DEPT PATHOL,IOWA CITY,IA 52242. ALAMAR BIOSCI INC,SACRAMENTO,CA 95834. JANSSEN RES FDN,B-2340 BEERSE,BELGIUM. AB BIODISK,S-17136 SOLNA,SWEDEN. UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET HOSP,LAB SERV,SAN ANTONIO,TX 78284. RP Rex, JH (reprint author), UNIV TEXAS,SCH MED,DEPT INTERNAL MED,CTR INFECT DIS,6431 FANNIN,1728 JFB,HOUSTON,TX 77030, USA. NR 8 TC 41 Z9 41 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD APR PY 1996 VL 34 IS 4 BP 816 EP 817 PG 2 WC Microbiology SC Microbiology GA UA683 UT WOS:A1996UA68300008 PM 8815089 ER PT J AU Singer, S Baldini, EH Demetri, GD Fletcher, JA Corson, JM AF Singer, S Baldini, EH Demetri, GD Fletcher, JA Corson, JM TI Synovial sarcoma: Prognostic significance of tumor size, margin of resection, and mitotic activity for survival SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID SOFT-TISSUE SARCOMAS; EXTREMITY; FEATURES AB Purpose: The present study serves to describe outcomes-based prognostic variables characteristic of synovial cell sarcoma. Patients and Methods: An analysis was performed of a prospectively compiled data base of 48 consecutive patients with extremity and truncal synovial sarcomas seen between 1966 and 1994. Results: No local recurrences were observed among 27 patients who presented with localized primary disease. Patients with synovial sarcomas less than 5 cm in size had a cancer-specific survival rate at 10 years of 100%, compared with a 10-year survival rate of 32% and 0% for those with sarcomas 5 to 10 cm and greater than 10 cm, respectively (P =.002). Patients with synovial sarcomas with less than 10 mitoses per 10 high-power fields (hpf) had a 10-year cancer-specific survival rate of 46%, compared with a 10-year survival rate of 14% for those with sarcomas with greater than 10 mitoses per 10 hpf (P =.04). Patients with a clean margin excision of sarcoma were found to have a 10-year caneer-specific survival rate of 43%, compared with 0% for those with microscopic positive margins (P =.03), Among 14 patients treated with neoadjuvant chemotherapy, seven (50%) had objective responses. Conclusion: Local control for patients with nonmetastatic disease was excellent. The overall cancer-specific survival rate for patients with localized synovial sarcoma was 34% at 10 years. Primary tumor size, margin of resection, and mean mitotic activity were prognostic factors for survival in synovial sarcoma. There was a high objective response rate to treatment with neoadjuvant chemotherapy; however, there were no detectable beneficial effects on survival in the subset of patients treated with chemotherapy versus nonrandomized patients who received no chemotherapy. Patients with synovial sarcomas greater than or equal to 5 cm in size, microscopic positive margins, and/or mean mitotic activity greater than 10 mitoses per 10 hpf should be targeted for new therapeutic studies. (C) 1996 by American Society of Clinical Oncology. C1 BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. DANA FARBER CANC INST,DEPT MED ONCOL,BOSTON,MA 02115. RP Singer, S (reprint author), BRIGHAM & WOMENS HOSP,DIV SURG ONCOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 27 TC 107 Z9 114 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1996 VL 14 IS 4 BP 1201 EP 1208 PG 8 WC Oncology SC Oncology GA UF068 UT WOS:A1996UF06800021 PM 8648375 ER PT J AU Gordon, LI Andersen, J Habermann, TM Winter, JN Glick, J Schilder, RJ Cassileth, P AF Gordon, LI Andersen, J Habermann, TM Winter, JN Glick, J Schilder, RJ Cassileth, P TI Phase I trial of dose escalation with growth factor support in patients with previously untreated diffuse aggressive lymphomas: Determination of the Maximum-tolerated dose of ProMACE-CytaBOM SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID NON-HODGKINS-LYMPHOMA; STANDARD REGIMEN CHOP; CHEMOTHERAPY; INTENSITY; CANCER AB Purpose: The aim of this study was to determine the maximum-tolerated dose (MTD) of cyclophosphamide, doxorubicin, etoposide, prednisone, bleomycin, cytarabine, methotrexate, and leucovorin (ProMACE-CytaBOM) when the myelotoxic drugs cyclophosphamide, doxorubicin, etoposide, and cytarabine are escalated. Patients and Methods: Thirty-eight eligible patients with diffuse aggressive non-Hodgkin's lymphoma were treated on a phase I trial of dose escalation using the ProMACE-CytaBOM regimen and granulocyte-macrophage colony-stimulating factor (GM-CSF; Schering, Kenilworth, NJ). Patients were treated with recombinant (r)GM-CSF 10 mu g/kg/d subcutaneouly from day 9 to 19. Twenty-seven patients had stage IV disease, four had stage III, and seven had bulky stage II. Half of the patients had bone marrow involvement. The median age was 45 years. Results: We found that the MTD was 200% for the escalated drugs in this regimen (although we never escalated above the MTD or defined by dose-limiting toxicity) and that the normalized dose-intensity (NDI; defined as the ratio of the received dose-intensity to the 100% dose-intensity of ProMACE-CytaBOM) decreased with each cycle and was lower for the day-8 drug (cytarabine) than for the day-1 drugs. The complete response (CR) rate was 66%, and 92% of patients who achieved CR are alive without disease with a median follow-up time for survival of 3.6 years. Conclusion: The MTD of cyclophosphamide, doxorubicin, etoposide, and cytarabine in the ProMACE-CytaBOM regimen given with growth factor support is 200%, and this dose should be tested in larger phase II trials. (C) 1996 by American Society of Clinical Oncology. C1 ROBERT H LURIE CANC CTR,CHICAGO,IL 60611. DANA FARBER CANC INST,BOSTON,MA 02115. MAYO CLIN,ROCHESTER,MN. UNIV PENN,MED CTR,PHILADELPHIA,PA 19104. FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. UNIV MIAMI,SYLVESTER CANC CTR,MIAMI,FL 33152. RP Gordon, LI (reprint author), NORTHWESTERN UNIV,SCH MED,DIV HEMATOL ONCOL,DEPT MED,303 E CHICAGO AVE,CHICAGO,IL 60611, USA. OI Gordon, Leo/0000-0003-1666-7064 FU NCI NIH HHS [CA13650, CA17145, CA23318] NR 13 TC 20 Z9 20 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1996 VL 14 IS 4 BP 1275 EP 1281 PG 7 WC Oncology SC Oncology GA UF068 UT WOS:A1996UF06800030 PM 8648384 ER PT J AU Haffajee, AD Socransky, SS Dibart, S Kent, RL AF Haffajee, AD Socransky, SS Dibart, S Kent, RL TI Response to periodontal therapy in patients with high or low levels of P-gingivalis, P-intermedia, P-nigrescens and B-forsythus SO JOURNAL OF CLINICAL PERIODONTOLOGY LA English DT Article DE periodontal disease; bacteria; treatment; antibiotics; diagnostics ID LOCALIZED JUVENILE PERIODONTITIS; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; REFRACTORY PERIODONTITIS; TETRACYCLINE; METRONIDAZOLE; ANTIBIOTICS; MICROBIOTA; LESIONS; SAMPLES; DISEASE AB In a previous study, subjects receiving either adjunctive tetracycline or Augmentin showed, on average, more attachment level gain 10 months posttherapy than subjects receiving either Ibuprofen or a placebo, although some subjects in each treatment group showed loss of attachment post-therapy. Since differences in treatment response might have been due to differences in the subgingival microbiota, the response to different therapies in subjects with different pre-therapy subgingival microbiotas was evaluated. 29 subjects exhibiting loss of attachment >2.5 mm at 1 or more sites during longitudinal monitoring were treated by modified Widman flap surgery at deep sites, subgingival scaling at all other sites and were randomly assigned one of the following agents: Augmentin, tetracycline, ibuprofen or a placebo. Treatment was completed within 30 days, during which time the subject took the assigned agent. Subgingival plaque samples were taken from the mesial surface of each tooth at each visit and evaluated for their content of 14 subgingival species including P. gingivalis, P. nigrescens, P. intermedia and B. forsythus using DNA probes. 18 subjects with mean counts >10(5) of 2 or more of these 4 species comprised the high test species group; 11 subjects with mean counts >10(5) of 0 or 1 of the species, the low test species group. Because this was a post-hoc analysis, the number of subjects in some of the treatment/test species groups was small. However, the 8 high test species subjects who received tetracycline showed the most attachment level gain (0.83+/-0.20 mm), while the 3 tetracycline-treated, low test species subjects showed minimal gain (0.05+/-0.28 mm) 10 months post-therapy. Low test species subjects receiving Augmentin (n=2) showed a mean gain in attachment of 0.67 (+/-0.59) mm. The mean % of sites showing either attachment gain or loss greater than or equal to 2 mm was computed for each treatment/test species group. High test species subjects receiving tetracycline exhibited the best ratio of gaining to losing sites (16.2), followed by low test species subjects receiving Augmentin (14.1). Periodontal pockets <7 mm pre-therapy in low test species subjects treated with Augmentin and high test species subjects treated with tetracycline showed attachment gain more frequently than attachment loss. The greatest proportion of gaining sites was seen at pockets >6 mm, particularly in subjects receiving adjunctive tetracycline. Overall, the data indicated that a gain in mean attachment level post-therapy was significantly associated (p<0.001) with an increase in C. ochracea accompanied by a decrease in B. forsythus, P. gingivalis, P. intermedia and P. nigrescens. The 4 test species were decreased more in subjects receiving tetracycline. In contrast, Augmentin appeared to be effective in decreasing the % sites colonized by A. actinomycetemcomitans and in increasing the proportion of sites colonized by C. ochracea. Knowledge of the baseline microbiota should improve the choice of an appropriate adjunctive antibiotic for periodontal therapy. C1 FORSYTH DENT CTR,DEPT BIOSTAT,BOSTON,MA 02115. RP Haffajee, AD (reprint author), FORSYTH DENT CTR,DEPT PERIODONTOL,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-04881] NR 27 TC 33 Z9 33 U1 2 U2 2 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6979 J9 J CLIN PERIODONTOL JI J. Clin. Periodontol. PD APR PY 1996 VL 23 IS 4 BP 336 EP 345 DI 10.1111/j.1600-051X.1996.tb00555.x PG 10 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA UK403 UT WOS:A1996UK40300006 PM 8739165 ER PT J AU Koran, LM McElroy, SL Davidson, JRT Rasmussen, SA Hollander, E Jenike, MA AF Koran, LM McElroy, SL Davidson, JRT Rasmussen, SA Hollander, E Jenike, MA TI Fluvoxamine versus clomipramine for obsessive-compulsive disorder: A double-blind comparison SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article ID SEROTONIN; DESIPRAMINE; INHIBITORS; FLUOXETINE; EFFICACY; PLACEBO; SCALE AB The efficacy and tolerability of fluvoxamine (100-300 mg/day) and clomipramine (100-250 mg/day) were compared in a randomized, double-blind, parallel-group study of 79 patients with obsessive-compulsive disorder (OCD) without coexisting major depression. After a 2-week placebo lead-in period, patients were randomized to fluvoxamine (37 patients) or clomipramine (42 patients) for 10 weeks. Efficacy was evaluated with the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), the National Institute of Mental Health Obsessive-Compulsive scale, and Patient and Clinical Global Improvement scales. Hamilton Rating Scale for Depression scores and somatic symptoms were also assessed. Seventy-eight percent of fluvoxamine patients and 64% of clomipramine patients completed the study. At the end of treatment, 56% of fluvoxamine patients were classified as responders (greater than or equal to 25% decrease in Y-BOCS score), compared with 54% of clomipramine patients. Both groups showed steady improvement throughout the study; no statistically significant differences were observed between the groups for any efficacy variable at any time. A similar percentage of patients in both groups withdrew because of adverse events. No serious adverse events related to drug occurred with either drug. Insomnia, nervousness, and dyspepsia were more statistically frequent with fluvoxamine; dry mouth and postural hypotension were more frequent with clomipramine. In this study, fluvoxamine and clomipramine were equally effective in reducing OCD symptoms over a 10-week treatment period but displayed different side effect profiles. C1 UNIV CINCINNATI COLL,COLL CINCINNATI,COLL MED,DEPT PSYCHIAT,BIOL RES PROGRAM,CINCINNATI,OH. DUKE UNIV,MED CTR,ANXIETY & TRAUMAT STRESS PROGRAM,DURHAM,NC. DUKE UNIV,MED CTR,DEPT PSYCHIAT & BEHAV SCI,DURHAM,NC. BUTLER HOSP,DEPT PSYCHIAT,PROVIDENCE,RI 02906. MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY. MT SINAI SCH MED,DEPT CLIN PSYCHOPHARMACOL,NEW YORK,NY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA. RP Koran, LM (reprint author), STANFORD UNIV,MED CTR,DEPT PSYCHIAT & BEHAV SCI,DEPT PSYCHIAT,ROOM 3362,STANFORD,CA 94305, USA. NR 35 TC 89 Z9 89 U1 6 U2 8 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD APR PY 1996 VL 16 IS 2 BP 121 EP 129 DI 10.1097/00004714-199604000-00004 PG 9 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA UD632 UT WOS:A1996UD63200004 PM 8690827 ER PT J AU Sachs, GS AF Sachs, GS TI Bipolar mood disorder: Practical strategies for acute and maintenance phase treatment SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Article; Proceedings Paper CT Meeting on Key Issues in the Diagnosis and Treatment of Bipolar Disorder CY JUL, 1995 CL CHICAGO, IL ID MANIC-DEPRESSIVE ILLNESS; LOW SERUM LEVELS; DOUBLE-BLIND; LITHIUM-CARBONATE; PROPHYLACTIC LITHIUM; IMIPRAMINE; CLONAZEPAM; SYMPTOMS; DISCONTINUATION; VALPROATE AB The chronic, complex, and episodic course of bipolar mood disorder presents a formidable challenge to the clinician making a treatment plan. Although numerous therapeutic agents are reported to be efficacious for one or more aspects of bipolar illness, treatment is seldom completely effective and is never curative. The goal of treatment is to modify the symptomatic expression of the illness with the result that fewer, briefer, and milder episodes occur. In pursuit of this goal, the use of multiple medications, polypharmacy, is the rule rather than the exception. This article offers recommendations for treatment strategies based on the phase and stage of the illness. The strategies are organized into algorithms that emphasize the use of mood-stabilizing medications as initial steps in a systematic, iterative approach to treatment. Practical issues related to the use of mood-stabilizing therapies are discussed. RP Sachs, GS (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114, USA. NR 85 TC 66 Z9 66 U1 2 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD APR PY 1996 VL 16 IS 2 SU 1 BP S32 EP S47 DI 10.1097/00004714-199604001-00005 PG 16 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA UE552 UT WOS:A1996UE55200006 PM 8707998 ER PT J AU Honrado, GI Johnson, RS Golombek, DA Spiegelman, BM Papaioannou, VE Ralph, MR AF Honrado, GI Johnson, RS Golombek, DA Spiegelman, BM Papaioannou, VE Ralph, MR TI The circadian system of c-fos deficient mice SO JOURNAL OF COMPARATIVE PHYSIOLOGY A-NEUROETHOLOGY SENSORY NEURAL AND BEHAVIORAL PHYSIOLOGY LA English DT Article DE circadian rhythm; gene targeting; phase shift; entrainment; light cycle ID SUPRACHIASMATIC NUCLEUS; GENE-EXPRESSION; LIGHT; HAMSTER; MOUSE; CLOCK; SENSITIVITY; PROTEINS; JUN AB We examined the role of c-fos in the synchronization of circadian rhythms to environmental light cycles using a line of gene-targeted mice carrying a null mutation at this locus. Circadian locomotor rhythms in mutants had similar periods as wild-type controls but took significantly longer than controls to entrain to 12:12 light-dark cycles. Light-induced phase shifts of rhythms in constant dark were attenuated in mutants although the circadian timing of phase delays and advances was not changed. A functional retinohypothalamic projection was indicated from behavioral results and light-induced jun-B expression in the SCN. The results indicate that while c-fos activation is not an absolute requirement for rhythm generation nor photic responses, it is required for normal entrainment of the mammalian biological clock. C1 UNIV TORONTO, DEPT PSYCHOL, TORONTO, ON M5S 1A1, CANADA. UNIV TORONTO, DEPT ZOOL, TORONTO, ON M5S 1A1, CANADA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT CELL BIOL, BOSTON, MA 02115 USA. TUFTS UNIV, SCH MED & VET MED, BOSTON, MA 02111 USA. OI Johnson, Randall/0000-0002-4084-6639; Golombek, Diego/0000-0002-6291-5586 FU NICHD NIH HHS [HD277295] NR 26 TC 59 Z9 61 U1 0 U2 3 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0340-7594 J9 J COMP PHYSIOL A JI J. Comp. Physiol. A -Neuroethol. Sens. Neural Behav. Physiol. PD APR PY 1996 VL 178 IS 4 BP 563 EP 570 PG 8 WC Behavioral Sciences; Neurosciences; Physiology; Zoology SC Behavioral Sciences; Neurosciences & Neurology; Physiology; Zoology GA TZ919 UT WOS:A1996TZ91900013 PM 8847666 ER PT J AU AlAlousi, S Carlson, JA Blessing, K Cook, M Karaoli, T Barnhill, RL AF AlAlousi, S Carlson, JA Blessing, K Cook, M Karaoli, T Barnhill, RL TI Expression of basic fibroblast growth factor in desmoplastic melanoma SO JOURNAL OF CUTANEOUS PATHOLOGY LA English DT Article ID ENDOTHELIAL-CELLS; MALIGNANT-MELANOMA; HUMAN MELANOCYTES; BFGF; LOCALIZATION; PROGRESSION; INDUCTION; LESIONS; INVITRO; GENES AB Basic fibroblast growth factor (bFGF) is an established growth factor for melanocytes and a potent angiogenic factor. The expression of bFGF was investigated in 23 desmoplastic melanomas. (DM) (12 males, median age 64 years, and 11 females, median age 54 years) by immunostaining of formalin-fixed, paraffin-embedded sections with high-affinity purified antibody raised against recombinant human bFGF (Scios Nova, Inc.). The tumors were characterized by level II invasion in 1 case (5%), level IV invasion in 11 cases (48%), level V invasion in 8 cases (35%), and indeterminate in 3 cases. bFGF expression was observed in 22 of 23 tumors (95%), either immune localized to tumor cell nuclei in 17 of 22 tumors (77%), or to the cytoplasm of tumor cells in 5 of 22 tumors (23%). Also in these cases, bFGF tvas strongly expressed in the nuclei of vascular endothelial cells. Maximal expression was noted in the peripheral blood vessels of 20 tumors (91%) versus intratumoral vessels of 13 DM (59%). In conclusion, the expression of predominantly nuclear bFGF by tumor cells in DM suggests a role in mediating the desmoplastic phenotype. In addition, the localization of bFGF to vascular endothelium, particularly at the periphery of the tumor, may be relevant to tumor angiogenesis. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02115. CHILDRENS HOSP,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. UNIV ABERDEEN,ABERDEEN,SCOTLAND. UNIV LONDON ST GEORGES HOSP,LONDON,ENGLAND. OI Carlson, John Andrew/0000-0002-6866-6314 NR 44 TC 24 Z9 26 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6987 J9 J CUTAN PATHOL JI J. Cutan. Pathol. PD APR PY 1996 VL 23 IS 2 BP 118 EP 125 DI 10.1111/j.1600-0560.1996.tb01284.x PG 8 WC Dermatology; Pathology SC Dermatology; Pathology GA UD477 UT WOS:A1996UD47700003 PM 8721445 ER PT J AU vanHoute, J Lopman, J Kent, R AF vanHoute, J Lopman, J Kent, R TI The final pH of bacteria comprising the predominant flora on sound and carious human root and enamel surfaces SO JOURNAL OF DENTAL RESEARCH LA English DT Article DE oral bacteria; dental plaque; dental caries; bacterial acid tolerance ID STREPTOCOCCUS-MUTANS; DENTAL PLAQUE; CONTINUOUS CULTURE; SELECTIVE MEDIUM; CARIES; ADAPTATION; DENTITION; RECOVERY; ETIOLOGY; SUCROSE AB Acidogenesis at low pH appears to be an important bacterial cariogenic trait. However, most information in this regard pertains to only a few of the acidogenic dental plaque bacteria. Therefore, the 'final' pH in sugar broth was determined for a wide variety of oral bacteria. Their source was: (1) carious material from advanced root lesions (ARL), (2) plaque from sound root surfaces of root-caries-free subjects (SRS), (3) plaque from ''white spot'' coronal lesions and sound coronal surfaces of caries-active subjects, and (4) plaque from sound coronal surfaces of caries-free subjects. Strains from groups 1 and 2 (ARL, 389 strains; SRS, 358 strains) were previously identified (van Houte et al., 1994) to the genus/species level and belonged to the predominant cultivable flora (PCF). Strains from groups 3 and 4 also belonged to the PCF but were not identified. All strains were placed in one of 4 final pH categories: < 4.2, 4.2 - 4.4, 4.4 - 4.6, and greater than or equal to 4.6. The main findings were: (1) ARL samples contained many strains with a final pH < 4.2 (mean percentage of 25.7). They included all strains of Lactobacillus and mutans streptococci (MS), most Bifidobacterium strains and non-mutans streptococci (non-MS), and about 20% of the Actinomyces strains. By contrast, SRS samples contained far fewer strains with a final pH < 4.2 (mean percentage of 8.4) which were nearly all non-MS. (2) Organisms with a final pH < 4.4 constituted mean percentages of 41.5 and 32.1 for the ARL and SRS samples, respectively. (3) The final pH distribution of strains in samples from coronal surfaces showed a tendency relative to caries activity (group 3 vs. group 4) similar to that for groups 1 and 2. Our findings further support the concept that increased cariogenic conditions are associated with increased proportions of organisms capable of acidogenesis at a low pH and that this shift involves organisms other than the MS and lactobacilli. C1 FORSYTH DENT CTR,DEPT CLIN TRIALS & HUMAN EXPERIMENTAT,BOSTON,MA 02115. RP vanHoute, J (reprint author), FORSYTH DENT CTR,DEPT ORAL MICROBIOL,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-07009] NR 27 TC 72 Z9 76 U1 2 U2 3 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD APR PY 1996 VL 75 IS 4 BP 1008 EP 1014 PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA VA158 UT WOS:A1996VA15800011 PM 8708129 ER PT J AU Gorski, PA AF Gorski, PA TI The extent and importance of research to developmental and behavioral pediatrics - Comment SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Editorial Material RP Gorski, PA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD APR PY 1996 VL 17 IS 2 BP 136 EP 136 DI 10.1097/00004703-199604000-00046 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA UF575 UT WOS:A1996UF57500020 ER PT J AU Biancone, L Andres, G Ahn, H Lim, A Dai, C Noelle, R Yagita, H DeMartino, C Stamenkovic, I AF Biancone, L Andres, G Ahn, H Lim, A Dai, C Noelle, R Yagita, H DeMartino, C Stamenkovic, I TI Distinct regulatory roles of lymphocyte costimulatory pathways on T helper type 2-mediated autoimmune disease SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID ANTI-CD2 MONOCLONAL-ANTIBODIES; CELL ACTIVATION; B-CELLS; INVIVO; IL-4; CD2; INDUCTION; PROTEIN; SIGNAL; MICE AB We assessed the role of CD40-CD40L, cytotoxic T lymphocyte (CTL)A4/CD28-B7s, and CD2-CD48/CD58 lymphocyte costimulatory pathways in the development of mercury chloride (HgCl2)-induced autoimmune disease in mice, which is believed to be mediated by T helper (Th) subset Th2. Inhibition of CD40-CD40L and CTLA4/CD28-B7s interactions by anti-CD40L antibody and soluble CTLA4-immunoglobulin (Ig) fusion protein, respectively, abrogated the autoimmune disease without affecting interleukin 4 (IL-4) production, showing the importance of physical contact between T and B lymphocytes in the Th2-mediated process. In contrast, two anti-CD2 antibodies that have been shown to induce immunosuppression of Th1-mediated events exacerbated the autoantibody response and augmented IgG1, IgE, and IL-4 production, transforming a mild mesangial glomerulopathy into a severe systemic immune complex disease. These observations demonstrate that manipulation of lymphocyte accessory counterreceptor interactions may affect the course of Th2-associated autoimmune disease and suggest that signals resulting from CD2 engagement may play an essential role in the regulation of the Th1-Th2 effector equilibrium. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02129. DARTMOUTH COLL SCH MED,DEPT MICROBIOL,LEBANON,NH 03756. JUNTENDO UNIV,SCH MED,DEPT IMMUNOL,BUNKYO KU,TOKYO 113,JAPAN. IST DERMATOL S MARIA & S GALLICANO,I-00041 ROME,ITALY. FU NCI NIH HHS [CA-55735]; NIDDK NIH HHS [DK-36807]; NIGMS NIH HHS [GM/AI-48614] NR 28 TC 54 Z9 54 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1996 VL 183 IS 4 BP 1473 EP 1481 DI 10.1084/jem.183.4.1473 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA UH144 UT WOS:A1996UH14400021 PM 8666905 ER PT J AU Kalams, SA Johnson, RP Dynan, MJ Hartman, KE Harrer, T Harrer, E Trocha, AK Blattner, WA Buchbinder, SP Walker, BD AF Kalams, SA Johnson, RP Dynan, MJ Hartman, KE Harrer, T Harrer, E Trocha, AK Blattner, WA Buchbinder, SP Walker, BD TI T cell receptor usage and fine specificity of human immunodeficiency virus 1-specific cytotoxic T lymphocyte clones: Analysis of quasispecies recognition reveals a dominant response directed against a minor in vivo variant SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID UNRELATED ALLOANTIGENS; INFECTED PERSONS; ALPHA-CHAIN; CONSERVATION; IMMUNIZATION; INDIVIDUALS; SEQUENCE; PEPTIDE; COMPLEX; PROTEIN AB Numerous virus-specific, class I-restricted cytotoxic T lymphocyte (CTL) epitopes have been identified, yet little information is available regarding the specificity of the CTL response in persons of the same human histocompatibility leukocyte antigen (HLA) type. In this study, the human immunodeficiency virus (HIV) 1 envelope-specific CTL response was evaluated in five HLA-B14-positive persons. CTL responses specific for a previously described nine-amino acid epitope in gp41 (aa 584-592, ERYLKDQQL) could be identified in all subjects, and CTL clones specific for this epitope could be isolated from four persons. Despite heterogeneous T cell receptor usage, the fine specificity of the clones was similar, as defined by recognition of alanine-substituted peptides as well as peptides representing natural HIV-1 sequence variants. Correlation with in vivo virus sequences revealed that the dominant species in two of the subjects represented poorly recognized variants, with a K-->Q substitution at amino acid 588, whereas no variants were observed in the other two subjects. Although clonal type-specific responses to these dominant variants could be identified, the magnitude of these responses remained small, and the dominant CTL response was directed at the minor in vivo variant. These studies indicate thai despite similar epitope-specific immunologic pressure in persons of the same HLA type, the in vivo quasispecies may differ, and that the major in vivo immune response to a given CTL epitope can be directed at a minor variant. C1 MASSACHUSETTS GEN HOSP, CTR AIDS RES, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, INFECT DIS UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, NEW ENGLAND REG PRIMATE CTR, BOSTON, MA 02114 USA. UNIV MARYLAND, SCH MED, INST HUMAN VIROL, BALTIMORE, MD 21201 USA. DEPT PUBL HLTH, AIDS OFF, SAN FRANCISCO, CA 94140 USA. FU NIAID NIH HHS [AI-45218, K08-AI-01273]; PHS HHS [R37-28568] NR 34 TC 51 Z9 51 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1996 VL 183 IS 4 BP 1669 EP 1679 DI 10.1084/jem.183.4.1669 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA UH144 UT WOS:A1996UH14400041 PM 8666925 ER PT J AU Jenike, MA AF Jenike, MA TI Psychiatric illnesses in the elderly: A review SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article ID NEUROLEPTIC MALIGNANT SYNDROME; PRIMARY DEGENERATIVE DEMENTIA; MONOAMINE-OXIDASE INHIBITORS; ORGANIC BRAIN DISEASE; ALZHEIMERS-DISEASE; ELECTROCONVULSIVE-THERAPY; BIPOLAR DISORDER; DOUBLE-BLIND; CLINICAL-DIAGNOSIS; DEPRESSED-PATIENTS AB Neuropsychiatric disorders in the elderly, such as dementia, depression, anxiety, and psychosis, may occur alone or in combination with neurologic or medical illness. Geriatricians must be familiar not only with diagnostic issues but also with treatment options and medication-induced alterations in mental status. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 125 TC 19 Z9 19 U1 2 U2 3 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD APR PY 1996 VL 9 IS 2 BP 57 EP 82 PG 26 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA UN567 UT WOS:A1996UN56700002 PM 8736587 ER PT J AU Gonzales, JJ Emmerich, AD Rauch, SL Stern, TA AF Gonzales, JJ Emmerich, AD Rauch, SL Stern, TA TI Management of the prescription-drug-dependent adult: Case of meprobamate abuse and its treatment SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article ID BENZODIAZEPINE DEPENDENCE; PSYCHIATRIC-DIAGNOSIS; MENTAL-DISORDERS; PRIMARY CARE; PREVALENCE; WITHDRAWAL; DEPRESSION; CLONAZEPAM; ANXIETY; ADDICTS AB Misuse of prescription drugs in the elderly can be a serious problem that is difficult to manage. Prescriptions for non-narcotic central nervous system (CNS) depressants (e.g., anxiolytics and sedative-hypnotics) are commonly written, and their use is associated with severe intoxication and withdrawal effects. The presence of comorbid psychiatric conditions (e.g., depression or panic disorder), for which these agents are prescribed frequently, complicates the clinical picture. This paper, using case examples of meprobamate abuse, describes how physicians can recognize, manage, and treat a patient who is abusing a non-narcotic CNS depressant. C1 GEORGETOWN UNIV,MED CTR,DEPT PSYCHIAT,WASHINGTON,DC 20057. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 30 TC 1 Z9 2 U1 2 U2 2 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD APR PY 1996 VL 9 IS 2 BP 91 EP 96 PG 6 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA UN567 UT WOS:A1996UN56700004 PM 8736589 ER PT J AU Glick, REL Sanders, KM Stern, TA AF Glick, REL Sanders, KM Stern, TA TI Failure to record delirium as a complication of intra-aortic balloon pump treatment: A retrospective study SO JOURNAL OF GERIATRIC PSYCHIATRY AND NEUROLOGY LA English DT Article ID PROSPECTIVE-PAYMENT; DIAGNOSIS; ACCURACY; CARE AB This study was conducted to determine whether or not diagnosis and treatment of delirium among patients treated with the intra-aortic balloon pump (IABP) correlates with the recording of this complication on discharge records. Since prior episodes of delirium are one of the few clear risk factors for future episodes of delirium, accurate recording of delirium on the discharge summary and list of discharge diagnoses is useful to clinicians. A retrospective review of the charts of all patients (N = 198) who underwent placement of an IABP during 1988; assessment of the type and frequency of medical and neuropsychiatric complications during IABP treatment; and comparison of chart review findings with the Massachusetts General Hospital's computer-generated Lists of discharge diagnoses for the same IABP-treated patients was completed. Only 12% of patients diagnosed and treated for delirium had delirium recorded as a discharge diagnosis. In contrast, 44% and 52% of patients who had been diagnosed and treated for cerebrovascular accident and pneumonia, respectively, had these diagnoses recorded among the discharge diagnoses. Receiving a discharge diagnosis of organic brain syndrome increased the likelihood that delirium was recorded as a discharge diagnosis. Delirium is underdiagnosed as a complication associated with IABP-treatment and is under-reported on the list of discharge diagnoses, even when it is diagnosed. Further study is warranted to determine if making the diagnosis of delirium during a patient's hospital course and recording its a complication at the time of discharge is translated into a higher level of preparedness by physicians during subsequent hospitalizations. C1 UNIV MICHIGAN,SCH MED,DEPT PSYCHIAT,ANN ARBOR,MI. HARVARD UNIV,SCH MED,PSYCHIAT CONSULTAT SERV,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 14 TC 14 Z9 14 U1 0 U2 0 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0891-9887 J9 J GERIATR PSYCH NEUR JI J. Geriatr. Psychiatry Neurol. PD APR PY 1996 VL 9 IS 2 BP 97 EP 99 PG 3 WC Geriatrics & Gerontology; Clinical Neurology; Psychiatry SC Geriatrics & Gerontology; Neurosciences & Neurology; Psychiatry GA UN567 UT WOS:A1996UN56700005 PM 8736590 ER PT J AU Kadiyala, RK Gelberman, RH Kwon, B AF Kadiyala, RK Gelberman, RH Kwon, B TI Basal joint arthrosis - Radiographic assessment of the trapezial space before and after ligament reconstruction and tendon interposition arthroplasty SO JOURNAL OF HAND SURGERY-BRITISH AND EUROPEAN VOLUME LA English DT Article AB A radiographic method was developed, the trapezial space ratio, for assessing the space occupied by the trapezium (a space defined by the distal scaphoid and thumb metacarpal base divided by the thumb proximal phalanx), This method was applied to 100 normal thumb radiographs and to the radiographs of 15 patients with symptomatic degenerative arthrosis of the thumb basal joint before and after operative treatment with ligamentous reconstruction and tendon interposition arthroplasty, The trapezial space ratio averaged 0.476 +/- 0.033 for radiographs of normal thumbs, 0.372 +/- 0.084 for the pre-operative radiographs of thumbs with symptomatic basal joint arthrosis, and 0.270 +/- 0.078 for the radiographs of thumbs following basal joint arthroplasty. A significant reduction in the trapezial space ratio was noted when values from arthritic thumbs were compared to those of normal thumbs (22%; P < 0.0001), A further reduction in the trapezial space ratio was noted when post-operative values were compared to pre-operative ones (27%; P < 0.0002). Comparing post-operative trapezial space ratio values to values obtained in normal thumbs, a reduction of 43% was found in those thumbs treated operatively, These finding indicate that the trapezial space is reduced significantly in thumbs with severe degenerative arthrosis compared to normal thumbs and that ligament reconstruction tendon interposition arthroplasty is not entirely successful in either restoring or maintaining the length of the thumb ray. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. NR 17 TC 31 Z9 33 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0266-7681 J9 J HAND SURG-BRIT EUR JI J. Hand Surg.-Br. Eur. Vol. PD APR PY 1996 VL 21B IS 2 BP 177 EP 181 DI 10.1016/S0266-7681(96)80093-3 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA UG230 UT WOS:A1996UG23000006 PM 8732396 ER PT J AU Harrer, T Harrer, E Kalams, SA Barbosa, P Trocha, A Johnson, RP Elbeik, T Feinberg, MB Buchbinder, SP Walker, BD AF Harrer, T Harrer, E Kalams, SA Barbosa, P Trocha, A Johnson, RP Elbeik, T Feinberg, MB Buchbinder, SP Walker, BD TI Cytotoxic T lymphocytes in asymptomatic long-term nonprogressing HIV-1 infection - Breadth and specificity of the response and relation to in vivo viral quasispecies in a person with prolonged infection and low viral load SO JOURNAL OF IMMUNOLOGY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; FINE SPECIFICITY; EPITOPES; CELLS; IDENTIFICATION; PEPTIDES; PROTEIN; REGION AB Although vigorous activated and memory CTL have been associated with HIV-1 infection, data are lacking regarding the breadth of epitopes recognized in a given individual and the relationship to the viral quasispecies present in vivo, In this study we performed a detailed analysis of the HIV-l-specific CTL response in a seropositive person with documented HIV-1 infection of 15 yr duration, stable CD4 counts above 500 cells/ml, and viral load persistently below 500 molecules of RNA/ml of plasma, Epitope mapping studies revealed the presence of HLA class I-restricted CTL responses to six different epitopes in p17, p24, RT, Env, and Nef, which conferred broadly cross-reactive recognition of reported HIV-1 variants. Sequence analysis of autologous viruses revealed the absence of immune escape variants within five of the six epitopes, Despite consistently low viral RNA levels in plasma and viral DNA levels in PBMC, in vivo-activated circulating CTL were detected against three of the epitopes, Five of the six epitopes, including the three dominant epitopes, have been detected in persons with progressive disease, suggesting that nonprogressors may not target unique epitopes, This study demonstrates that HIV-1-specific CTL can be highly activated and broadly directed in the setting of an extremely low viral load, and that neither high viral load nor antigenic diversity is required for the generation of a multispecific CTL response, Although the detection of strong CTL responses, low viral load, and lack of immune escape are consistent with the hypothesis that CTL may contribute to lack of disease progression in this individual, the contribution of these responses to maintenance of the asymptomatic state remains to be determined. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR AIDS RES,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,CTR AIDS RES,SAN FRANCISCO,CA 94141. UNIV CALIF SAN FRANCISCO,GLADSTONE INST CARDIOVASC DIS,SAN FRANCISCO,CA 94141. DEPT PUBL HLTH,AIDS OFF,SAN FRANCISCO,CA 94140. OI Elbeik, Tarek/0000-0001-5983-0867 NR 39 TC 281 Z9 285 U1 0 U2 4 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1996 VL 156 IS 7 BP 2616 EP 2623 PG 8 WC Immunology SC Immunology GA UB155 UT WOS:A1996UB15500041 PM 8786327 ER PT J AU Krueger, GG Liimatta, AP Jorgensen, CM Morgan, JR AF Krueger, GG Liimatta, AP Jorgensen, CM Morgan, JR TI Prolongation of genetically modified human fibroblasts in culture in an extracellular nylon matrix enhances survival in vivo. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV UTAH,HLTH SCI CTR,DEPT MED,DIV DERMATOL,SALT LAKE CITY,UT 84132. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURN INST,SURG SERV,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 4 EP 4 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700047 ER PT J AU Morgan, JR Eming, SE Medalie, DA Wiley, HS Krueger, GG AF Morgan, JR Eming, SE Medalie, DA Wiley, HS Krueger, GG TI Targeted expression of EGF and IGF-1 to human keratinocytes: Modification of the autocrine control of keratinocyte proliferation SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,SHRINERS BURNS INST,MASSACHUSETTS GEN HOSP,SURG SERV,CAMBRIDGE,MA 02138. UNIV UTAH,DEPT PATHOL,SALT LAKE CITY,UT. UNIV UTAH,DIV DERMATOL,SALT LAKE CITY,UT. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 89 EP 89 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700129 ER PT J AU Torji, H Hosoi, J Moro, O Lerner, EA Xu, S Takashima, A Granstein, RD AF Torji, H Hosoi, J Moro, O Lerner, EA Xu, S Takashima, A Granstein, RD TI Langerhans cells and nerves: Further support for a functional relationship. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA. UNIV TEXAS,SW MED CTR,DEPT DERMATOL,DALLAS,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 110 EP 110 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700154 ER PT J AU Granstein, RD Torii, H Asahina, ZYA Xu, S Takashima, A Fox, F Rook, AH Hosoi, J AF Granstein, RD Torii, H Asahina, ZYA Xu, S Takashima, A Fox, F Rook, AH Hosoi, J TI Regulation of cytokine expressions by calcitonin gene-related peptide (CGRP). SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV TEXAS,SW MED CTR,DALLAS,TX 75235. UNIV PENN,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 157 EP 157 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700199 ER PT J AU Moro, O Ohnuma, M Wakita, K Tajima, M Lerner, EA AF Moro, O Ohnuma, M Wakita, K Tajima, M Lerner, EA TI Receptors for the cutaneous vasodilator maxadilan are present in brain and neuro-derived cell lines. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. SHISEIDO LIFE SCI LABS,KANAGAWA,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 178 EP 178 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700221 ER PT J AU Langley, RGB Rajadhyaksha, M Dwyer, PJ Anderson, RR Sober, AJ AF Langley, RGB Rajadhyaksha, M Dwyer, PJ Anderson, RR Sober, AJ TI Confocal scanning laser microscopy of pigmented skin lesions SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,DEPT DERMATOL,BOSTON,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 185 EP 185 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700225 ER PT J AU Rutberg, SE Saez, E Spiegelman, B Yuspa, SH AF Rutberg, SE Saez, E Spiegelman, B Yuspa, SH TI Negative regulation of AP-1 transcriptional activity in differentiating mouse keratinocytes SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 NCI,CELLULAR CARCINOGENESIS & TUMOR PROMOT LAB,BETHESDA,MD 20205. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 196 EP 196 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700239 ER PT J AU Firooz, A Dowlati, Y Haider, N Ahmed, AR AF Firooz, A Dowlati, Y Haider, N Ahmed, AR TI Analysis of the nucleotide sequences of the DQB allele in patients with pemphigus vulgaris and their relatives. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 CTR RES & EDUC SKIN DIS,TEHRAN,IRAN. CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 252 EP 252 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700294 ER PT J AU Mobini, N Yunis, JJ Firooz, A Dowlati, Y Bahar, K Yunis, E Ahmed, AR AF Mobini, N Yunis, JJ Firooz, A Dowlati, Y Bahar, K Yunis, E Ahmed, AR TI Identical MHC markers in Iranian and Ashkenazi Jewish pemphigus vulgaris patients. Possible common ancestral origin. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 CTR BLOOD RES,BOSTON,MA. SKIN DIS RES CTR,TEHRAN,IRAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 253 EP 253 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700295 ER PT J AU Tyagi, SR Bhol, K Natarajan, K Nagarwalla, N Ahmed, AR AF Tyagi, SR Bhol, K Natarajan, K Nagarwalla, N Ahmed, AR TI Use of recombinant pemphigus vulgaris antigen in development of ELISA and IB assays to detect pemphigus vulgaris autoantibodies SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 254 EP 254 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700298 ER PT J AU Bhol, K Goss, L Tyagi, SR LivirRallatos, C Foster, CS Ahmed, AR AF Bhol, K Goss, L Tyagi, SR LivirRallatos, C Foster, CS Ahmed, AR TI Partial characterization of oral pemphigoid antigen. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CTR BLOOD RES,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 255 EP 255 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700296 ER PT J AU Hameed, A Khan, AA Rehman, S Yunis, JJ Yunis, EJ Ahmed, AR AF Hameed, A Khan, AA Rehman, S Yunis, JJ Yunis, EJ Ahmed, AR TI MHC class II genes in Rawalpindi, Pakistan and non-Jewish Caucasian patients in Boston with pemphigus vulgaris. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR BLOOD RES,BOSTON,MA 02115. ARMY MED COLL,RAWALPINDI,PAKISTAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 256 EP 256 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700299 ER PT J AU Hibino, T Takahashi, T Matsuda, Y Baciu, PC Baden, HP Goetinck, PF AF Hibino, T Takahashi, T Matsuda, Y Baciu, PC Baden, HP Goetinck, PF TI Cloning of two distinct types of psoriastatin cDNAs from psoriatic epidermis. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 SHISEIDO RES CTR,YOKOHAMA,KANAGAWA,JAPAN. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 414 EP 414 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700456 ER PT J AU Gonzalez, S Nguyen, CB Flotte, T Gillies, R Kollias, N AF Gonzalez, S Nguyen, CB Flotte, T Gillies, R Kollias, N TI Fluorescence based assessment of retinoid-induced reactions with special emphasis on comedolytic activity. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 426 EP 426 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700468 ER PT J AU Gonzalez, S AlcarazMartinez, MV Flotte, T Diaz, F deVargas, IP Kollias, N AF Gonzalez, S AlcarazMartinez, MV Flotte, T Diaz, F deVargas, IP Kollias, N TI Retinoid-induced changes of cutaneous cytogenetic behavior. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. UNIV MALAGA,FAC MED,MALAGA,SPAIN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 427 EP 427 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700469 ER PT J AU Oureshi, AA Bello, YM Lerner, EA AF Oureshi, AA Bello, YM Lerner, EA TI Langerhans cells produce nitric oxide, a toxin for melanocytes. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 454 EP 454 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700496 ER PT J AU Oureshi, AA Moro, O Youssef, DE Lerner, EA AF Oureshi, AA Moro, O Youssef, DE Lerner, EA TI Expression of adrenergic receptors on Langerhans cells suggests a role for stress in skin disease. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 455 EP 455 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700495 ER PT J AU Bello, YM Qureshi, AA Ordonez, C Lerner, EA AF Bello, YM Qureshi, AA Ordonez, C Lerner, EA TI Melanophores express the receptor for pituitary adenylate cyclase activating peptide. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 478 EP 478 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700520 ER PT J AU Rajadhyaksha, M Ugent, SJ Langley, RGB Dwyer, PJ Anderson, RR Webb, RH AF Rajadhyaksha, M Ugent, SJ Langley, RGB Dwyer, PJ Anderson, RR Webb, RH TI Confocal scanning laser microscopy of human skin lesions in vivo. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,DEPT DERMATOL,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 506 EP 506 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700549 ER PT J AU Smith, SL Drake, LA Scher, RK Smith, EB Faich, GA Hong, JJ Stiller, MJ AF Smith, SL Drake, LA Scher, RK Smith, EB Faich, GA Hong, JJ Stiller, MJ TI A multicenter study assessing the effect of onychomycosis on quality of life including functional, psychosocial and economic aspects. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. COLUMBIA UNIV,NEW YORK,NY. UNIV TEXAS,MED BRANCH,DEPT DERMATOL,GALVESTON,TX 77550. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 517 EP 517 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700558 ER PT J AU Amano, S Hibino, T Nishiyama, T Burgeson, RE AF Amano, S Hibino, T Nishiyama, T Burgeson, RE TI The laminin 5 synthesis and extracellular processing by human keratinocytes. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA. SHISEIDO RES CTR,YOKOHAMA,KANAGAWA,JAPAN. RI Nishiyama, Toshio/C-5434-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 536 EP 536 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700578 ER PT J AU Maytin, EV Habener, JF AF Maytin, EV Habener, JF TI Regulation of the mouse keratin K10 gene promoter by transcription factors of the CAAT-enhancer binding protein (C/EBP) family SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 605 EP 605 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700643 ER PT J AU Bello, YM Youssef, DE Lerner, EA AF Bello, YM Youssef, DE Lerner, EA TI Partial characterizations of a growth factor for Xenopus melanophores SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 630 EP 630 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700670 ER PT J AU Barba, A Yan, Z Beissert, S Granstein, RD AF Barba, A Yan, Z Beissert, S Granstein, RD TI Presentation of tumor-associated antigens by epidermal cells for in vivo anti-tumor immunity: Temporal relationship to tumor challenge. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 704 EP 704 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700745 ER PT J AU Yan, Z Lonati, A Beissert, S Granstein, RD AF Yan, Z Lonati, A Beissert, S Granstein, RD TI Presentation of tumor-associated antigens by dermal antigen presenting cells. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 705 EP 705 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700743 ER PT J AU Lohati, A Beissert, S Yan, Z Mohammad, T Morrison, H Granstein, RD AF Lohati, A Beissert, S Yan, Z Mohammad, T Morrison, H Granstein, RD TI Cis-urocanic acid (cis-UCA) inhibition of presentation of tumor-associated antigens (TAA) by epidermal cells (EC) may not be mediated by prostaglandins (PG) or interactions with H1 or H2 histamine receptors. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. PURDUE UNIV,DEPT CHEM,W LAFAYETTE,IN 47907. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 767 EP 767 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700804 ER PT J AU Fox, FE Kubin, M Cassin, M Niu, Z Hosoi, J Torji, H Granstein, RD Trinchieri, G Rook, AH AF Fox, FE Kubin, M Cassin, M Niu, Z Hosoi, J Torji, H Granstein, RD Trinchieri, G Rook, AH TI Calcitonin gene related peptide (CGRP) suppresses proliferation and antigen presentation by human PBMC: Effects on B7, interleukin-10 and interleukin-12. SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 UNIV PENN,WISTAR INST,DEPT DERMATOL,PHILADELPHIA,PA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 785 EP 785 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700822 ER PT J AU Beissert, S Dranoff, G Torji, H Hosoi, J Mulligan, RC Granstein, RD AF Beissert, S Dranoff, G Torji, H Hosoi, J Mulligan, RC Granstein, RD TI Increased contact (CHS) and delayed-type hypersensitivity (DTH) responses in granulocyte-macrophage colony-stimulating factor (GM-CSF)-deficient mice SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,WHITEHEAD INST BIOMED RES,DANA FARBER CANC INST,CUTANEOUS BIOL RES CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 818 EP 818 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700859 ER PT J AU Carder, KR Smith, SL Hillson, EM Stiller, MJ Kollias, N Gillies, R Siskin, SB Drake, LA AF Carder, KR Smith, SL Hillson, EM Stiller, MJ Kollias, N Gillies, R Siskin, SB Drake, LA TI A randomized, double-blind, parallel group, dose-ranging comparison of the efficacy and safety of calcipotriene solution in the treatment of scalp psoriasis SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1996 VL 106 IS 4 BP 844 EP 844 PG 1 WC Dermatology SC Dermatology GA UC787 UT WOS:A1996UC78700884 ER PT J AU Miller, SPF Zirzow, GC Doppelt, SH Brady, RO Barton, NW AF Miller, SPF Zirzow, GC Doppelt, SH Brady, RO Barton, NW TI Analysis of the lipids of normal and Gaucher bone marrow SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Article ID MACROPHAGE-TARGETED GLUCOCEREBROSIDASE; ENZYME REPLACEMENT THERAPY; SKELETAL COMPLICATIONS; MAGNETIC-RESONANCE; DISEASE; INVOLVEMENT; LEUKEMIA; CT AB Quantitative chemical shift magnetic resonance imaging (QCSI) is currently being utilized for measuring the extent of bone marrow involvement and its response to enzyme replacement therapy in patients with Gaucher's disease. Quantitation of the major lipid species in human bone marrow is required to accurately interpret QCSI data on bone marrow composition. The major lipid species in bone marrow specimens from normal individuals and from patients with type 1 Gaucher's disease were analyzed by thin-layer and high-pressure liquid chromatography. In normal marrow (N = 5), triglycerides were by far the most abundant lipid (278 +/- 70 mg/gm wet wt), with other non-polar lipids and phospholipids totaling less than 20 mg/gm wet weight.-The concentration of glucocerebroside in normal marrow was 0.061 +/- 0.06 mg/gm wet weight. Gaucher marrow (N = 9) had dramatically lower triglyceride levels (51 +/- 53 mg/gm wet wt), and as expected, it had markedly elevated levels of glucocerebroside (7.1 +/- 3.4 mg/gm wet wt). The other major non-polar lipids and phospholipids were measured in selected specimens, but none were found that differed so profoundly between normal and Gaucher's disease. These data support a model of bone marrow alteration in Gaucher's disease in which triglyceride rich adipocytes are progressively replaced by storage cells, leading to an overall reduction in total lipid content. This phenomenon provides an explanation for the changes in proton signal intensity observed in QCSI studies of Gaucher bone marrow. C1 NINCDS,NIH,DEV & METAB NEUROL BRANCH,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02114. NR 37 TC 26 Z9 26 U1 1 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-2143 J9 J LAB CLIN MED JI J. Lab. Clin. Med. PD APR PY 1996 VL 127 IS 4 BP 353 EP 358 DI 10.1016/S0022-2143(96)90183-3 PG 6 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA UC790 UT WOS:A1996UC79000007 PM 8656038 ER PT J AU Cacciola, JS Rutherford, MJ Alterman, AI McKay, JR Snider, EC AF Cacciola, JS Rutherford, MJ Alterman, AI McKay, JR Snider, EC TI Personality disorders and treatment outcome in methadone maintenance patients SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID ADDICTION SEVERITY INDEX; SUBSTANCE-ABUSERS; OPIATE ADDICTS; PREDICTOR AB This study examined the relationship between personality disorders (PDs) and 7-month treatment outcome in 197 men admitted to methadone maintenance. Subjects reported pervasive improvement, and the amount of improvement did not significantly differ for those subjects with and without PDs. PD subjects entered treatment with more severe self-reported drug, alcohol, psychiatric, and legal problems, and despite progress, remained more problematic in those areas relative to subjects without PDs. Subjects with antisocial PD had admission and 7-month problem status similar to subjects with other PDs. The 7-month urinalysis results for opiates and cocaine showed no significant differences between subjects with and without PDs. Fewer PD subjects stayed in treatment continuously for the 7-month period. Several cluster B PDs--borderline, antisocial, and histrionic-predicted poorest overall outcomes. Methadone-maintained patients with PDs may warrant additional treatment services if they are to approach the functional level of patients without PDs. C1 UNIV PENN,SCH MED,PHILADELPHIA VET AFFAIRS MED CTR,CTR STUDIES ADDICT,PHILADELPHIA,PA 19104. FU NIDA NIH HHS [R01 DA-05858-04, DA05186] NR 26 TC 75 Z9 75 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD APR PY 1996 VL 184 IS 4 BP 234 EP 239 DI 10.1097/00005053-199604000-00006 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA UG274 UT WOS:A1996UG27400006 PM 8604033 ER PT J AU Widnell, KL Chen, JS Iredale, PA Walker, WH Duman, RS Habener, JF Nestler, EJ AF Widnell, KL Chen, JS Iredale, PA Walker, WH Duman, RS Habener, JF Nestler, EJ TI Transcriptional regulation of CREB (cyclic AMP response element-binding protein) expression in CATH.a cells SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE cyclic AMP response element-binding protein; CATH.a cells; gene transcription regulation; cyclic AMP pathway; locus coeruleus ID GENE-TRANSCRIPTION; AUTOREGULATION; ACTIVATION; PROMOTER AB We have recently demonstrated that mRNA expression of cyclic AMP (cAMP) response element-binding protein (CREB) is down-regulated in CATH.a cells (a neural-derived cell line) by activation of the cAMP pathway. We now demonstrate that this down-regulation can be accounted for by a decrease in the rate of CREB gene transcription. It was found that cycloheximide, a protein synthesis inhibitor, prevented the forskolin-induced decrease in CREB mRNA levels in CATH.a cells. Nuclear run-on assays demonstrated that forskolin decreased the rate of CREB transcription by close to 50%. Moreover, forskolin decreased chloramphenicol acetyltransferase (CAT) activity in CATH.a cells transiently transfected with a construct containing 1,240 bp of CREB promoter fused to a CAT reporter plasmid. Possible mechanisms by which activation of the cAMP pathway leads to a decrease in CREB gene transcription are discussed. C1 YALE UNIV,SCH MED,CONNECTICUT MENTAL HLTH CTR,DEPT PSYCHIAT,MOL PSYCHIAT LAB,NEW HAVEN,CT 06508. YALE UNIV,SCH MED,DEPT PHARMACOL,NEW HAVEN,CT 06508. MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. FU NIDA NIH HHS [DA 08227, DA A00203] NR 16 TC 19 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD APR PY 1996 VL 66 IS 4 BP 1770 EP 1773 PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA UA119 UT WOS:A1996UA11900054 PM 8627337 ER PT J AU Buchanan, L Hildebrandt, N MacKinnon, GE AF Buchanan, L Hildebrandt, N MacKinnon, GE TI Phonological processing of nonwords in deep dyslexia: Typical and independent? SO JOURNAL OF NEUROLINGUISTICS LA English DT Article ID WORD RECOGNITION; PATIENT; PRINT; SOUND AB Patients with acquired deep dyslexia are unable to read nonwords aloud. The deficit has therefore been attributed to damage in nonlexical phonological processing. Buchanan, Hildebrandt and MacKinnon [5 Journal of Neurolingistics 8, 163-182, 1994] demonstrated that a deep dyslexic patient could process nonword phonology in two implicit tests. The generality of this claim is examined by replicating the Buchanan et al. experiments with two other deep dyslexic patients. Dissociations between Lexical and nonlexical processing are examined by manipulating nonword phonology in a task that does not require lexical analysis. The results suggest that sensitivity to nonword phonology in deep dyslexia is common and is distinct from a purely lexical analysis. Copyright (C) 1996 Elsevier Science Ltd C1 UNIV WATERLOO,DEPT PSYCHOL,WATERLOO,ON N2L 3G1,CANADA. MASSACHUSETTS GEN HOSP,NEUROPSYCHOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP Buchanan, L (reprint author), HOSP SICK CHILDREN,DEPT PSYCHOL,555 UNIV AVE,TORONTO,ON M5G 1X8,CANADA. NR 31 TC 15 Z9 16 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0911-6044 J9 J NEUROLINGUIST JI J. Neurolinguist. PD APR PY 1996 VL 9 IS 2 BP 113 EP 133 DI 10.1016/0911-6044(96)00001-2 PG 21 WC Linguistics; Neurosciences; Psychology, Experimental SC Linguistics; Neurosciences & Neurology; Psychology GA UY490 UT WOS:A1996UY49000004 ER PT J AU Macaruso, P Locke, JL Smith, T Powers, S AF Macaruso, P Locke, JL Smith, T Powers, S TI Short-term memory and phonological coding in developmental dyslexia SO JOURNAL OF NEUROLINGUISTICS LA English DT Article ID READING-DISABLED-CHILDREN; LEARNING-DISABILITIES; WORKING MEMORY; WORD-LENGTH; BEGINNING READERS; POOR READERS; PHONETIC MEMORY; YOUNG-CHILDREN; SERIAL-RECALL; SPEECH RATE AB In this study we examined the extent to which good and poor readers make use of phonological codes on a short-term memory task with nameable pictures. We compared performance for items that have short non-rhyming names with items that have short rhyming names and items with long non-rhyming names. Although the good readers outperformed the poor readers, both groups revealed evidence of phonological coding. The good readers showed significant rhyme and word-length effects, while the poor readers produced a significant rhyme effect. Serial position analyses revealed that the poor readers made use of phonological codes for initial items only, whereas the good readers showed evidence of phonological coding for items at all serial positions. In the General Discussion we consider possible reasons why poor readers fail to show evidence of phonological coding at later serial positions. Copyright (C) 1996 Elsevier Science Ltd RP Macaruso, P (reprint author), MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,NEUROLINGUIST LAB,BOSTON,MA 02114, USA. NR 59 TC 6 Z9 6 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0911-6044 J9 J NEUROLINGUIST JI J. Neurolinguist. PD APR PY 1996 VL 9 IS 2 BP 135 EP 146 DI 10.1016/0911-6044(95)00008-9 PG 12 WC Linguistics; Neurosciences; Psychology, Experimental SC Linguistics; Neurosciences & Neurology; Psychology GA UY490 UT WOS:A1996UY49000005 ER PT J AU Christie, RH Chung, H Rebeck, GW Strickland, D Hyman, BT AF Christie, RH Chung, H Rebeck, GW Strickland, D Hyman, BT TI Expression of the very low-density lipoprotein receptor (VLDL-r), an apolipoprotein-E receptor, in the central nervous system and in Alzheimer's disease SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE Alzheimer's disease; ApoE; apolipoprotein receptors; VLDL receptor ID AMYLOID-BETA-PEPTIDE; TYPE-4 ALLELE; PROTEIN; BINDING; IMMUNOREACTIVITY; DIAGNOSIS; MICROGLIA; DEPOSITS; CORTEX AB The very low density lipoprotein receptor (VLDL-r) is a cell-surface molecule specialized for the internalization of multiple diverse ligands, including apolipoprotein E (apoE)-containing lipoprotein particles, via clathrin-coated pits. Its structure is similar to the low-density lipoprotein receptor (LDL-r), although the two have substantially different systemic distributions and regulatory pathways. The present work examines the distribution of VLDL-r in the central nervous system (CNS) and in relation to senile plaques in Alzheimer disease (AD). VLDL-r is present on resting and activated microglia, particularly those associated with senile plaques (SPs). VLDL-r immunoreactivity is also found in cortical neurons. Two exons of VLDL-r mRNA are differentially spliced in the mature receptor mRNA. One set of splice forms gives rise to receptors containing (or lacking) an extracellular O-linked glycosylation domain near the transmembrane portion of the molecule. The other set of splice forms appears to be brain-specific, and is responsible for the presence or absence of one of the cysteine-rich repeat regions in the binding region of the molecule. Ratios of the receptor variants generated from these splice forms do not differ substantially across different cortical areas or in AD. We hypothesize that VLDL-r might contribute to metabolism of apoE and apoE/A beta complexes in the brain. Further characterization of apoE receptors in Alzheimer brain may help lay the groundwork for understanding the role of apoE in the CNS and in the pathophysiology of AD. C1 MASSACHUSETTS GEN HOSP,SERV NEUROL,BOSTON,MA 02114. AMER RED CROSS,ROCKVILLE,MD 20855. FU NIA NIH HHS [AG08487, AG12406]; NIGMS NIH HHS [GM42581] NR 43 TC 89 Z9 91 U1 0 U2 1 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD APR PY 1996 VL 55 IS 4 BP 491 EP 498 DI 10.1097/00005072-199604000-00012 PG 8 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA UE382 UT WOS:A1996UE38200012 PM 8786409 ER PT J AU Niethammer, M Kim, E Sheng, M AF Niethammer, M Kim, E Sheng, M TI Interaction between the C terminus of NMDA receptor subunits and multiple members of the PSD-95 family of membrane-associated guanylate kinases SO JOURNAL OF NEUROSCIENCE LA English DT Article DE NMDA receptor; PSD-95; PDZ domain; yeast two-hybrid system; guanylate kinase; cytoskeleton; postsynaptic density ID TUMOR-SUPPRESSOR PROTEIN; POTASSIUM-CHANNEL; MOLECULAR-CLONING; SEPTATE JUNCTIONS; DROSOPHILA; HOMOLOG; BRAIN; GENE AB Selective concentration and anchoring of ionotropic receptors at the synapse is essential for neuronal signaling. Little is known about the molecules that mediate receptor clustering in the CNS. With use of the yeast two-hybrid system to screen a rat brain cDNA library and by in vitro binding assays, we have identified an interaction between NMDA receptor subunits 2A and 2B (NR2A and NR2B) and three distinct members of the PSD-95/SAP90 family of membrane-associated putative guanylate kinases. The interaction is mediated by binding of the C terminus of the NMDA receptor subunits to the first two PDZ (also known as GLGF or DHR) domains of PSD-95/SAP90, an abundant synaptic protein associated with the membrane cytoskeleton. PSD-95 is also known to bind and cluster Shaker-type voltage-gated K+ channels. Similarities between the C termini of NR2 subunits and K+ channels suggest a common C-terminal binding motif for PDZ domains. These data suggest that PDZ domains can function as modules for protein-protein interactions. Members of the PSD-95 family might serve to anchor NMDA receptors to the submembrane cytoskeleton and aid in the assembly of signal transduction complexes at postsynaptic sites. C1 HARVARD UNIV, SCH MED,MASSACHUSETTS GEN HOSP, HOWARD HUGHES MED INST,DEPT NEUROBIOL, BOSTON, MA 02114 USA. RI Kim, Eunjoon/C-1566-2011 NR 51 TC 544 Z9 554 U1 0 U2 11 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR 1 PY 1996 VL 16 IS 7 BP 2157 EP 2163 PG 7 WC Neurosciences SC Neurosciences & Neurology GA UA742 UT WOS:A1996UA74200001 PM 8601796 ER PT J AU Didier, M Bursztajn, S Adamec, E Passani, L Nixon, RA Coyle, JT Wei, JY Berman, SA AF Didier, M Bursztajn, S Adamec, E Passani, L Nixon, RA Coyle, JT Wei, JY Berman, SA TI DNA strand breaks induced by sustained glutamate excitotoxicity in primary neuronal cultures SO JOURNAL OF NEUROSCIENCE LA English DT Article DE excitotoxicity; DNA damage; necrosis; apoptosis; NMDA receptor; glutamate transporter; cerebellar granule cells; primary cultures; nick translation; TUNEL labeling ID CEREBELLAR GRANULE CELLS; INSITU NICK TRANSLATION; AMINO-ACID RELEASE; RAT-BRAIN; NITRIC-OXIDE; NEURODEGENERATIVE DISORDERS; APOPTOSIS; NEUROTOXICITY; INVITRO; DEATH AB We developed a new approach to study single- and double-stranded DNA breaks during chronic, moderate excitotoxicity resulting from the inhibiton of the glutamate transporter in cerebellar granule cell primary cultures. A 24 hr treatment of 2-week-old cultures with L-alpha-amino adipate (LAA), an inhibitor of the cerebellar glutamate uptake transporter, caused a gradual extracellular accumulation of endogenous glutamate that induced reversible morphological change of granule neurons but no neuronal cell death despite sustained, but moderate, elevations of the free intracellular calcium concentrations. Nick translation experiments on isolated nuclei or cells from cerebellar cultures chronically exposed to LAA revealed increased radioactive nucleotide incorporation indicative of DNA nicking. This LAA effect was dose-dependent and suppressed by NMDA receptor antagonists. Cultures treated for 24 hr with LAA and subjected to in situ nick translation showed an intense nuclear labeling of neurons but not glia, which could be abolished by MK801. A similar labeling was also observed in altered nuclei of granule neurons acutely exposed to high glutamate concentrations or undergoing an apoptotic cell death. Although the TUNEL labeling method detected no DNA double-strand breaks in LAA-treated cerebellar cultures, it displayed clear evidence of DNA damage during acute glutamate excitotoxicity or during apoptosis. However, Southern blot analysis of nuclear DNA revealed a DNA laddering only in apoptotic cell death. Our results demonstrate that DNA damage, characterized by DNA single-strand breaks, is an early event in chronic, moderate excitotoxicity. This type of DNA degradation, which appears before any nuclear morphological changes, is distinct from the massive DNA single- and/or double-strand damages observed during acute glutamate excitotoxicity or apoptosis. C1 MCLEAN HOSP,LABS MOLEC NEUROSCI,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,LAB MOLEC & DEV NEUROSCI,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DIV AGING,BOSTON,MA 02115. NR 60 TC 124 Z9 124 U1 2 U2 4 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD APR 1 PY 1996 VL 16 IS 7 BP 2238 EP 2250 PG 13 WC Neurosciences SC Neurosciences & Neurology GA UA742 UT WOS:A1996UA74200009 PM 8601804 ER PT J AU Sakas, DE Whittaker, K Abbasi, KH Zervas, NT AF Sakas, DE Whittaker, K Abbasi, KH Zervas, NT TI Experimental microneurosurgery of the trigeminal nerve: Surgical technique for ganglionectomy and rhizotomy in the cat SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE trigeminal nerve; ganglionectomy; rhizotomy; surgery; (cat) ID VASCULAR HEADACHES; PAIN MECHANISMS; SUBSTANCE-P; DURA MATER; BLOOD; HYPERTENSION AB The techniques of two experimental surgical operations on the trigeminal nerve are described, namely, excision of the trigeminal ganglion (ganglionectomy) and division of the trigeminal root (rhizotomy), in the cat. These techniques have been developed with the specific aims of achieving the trigeminal lesion and also preserving a satisfactory postoperative quality of life for the animal in order to make it possible to study the long-term effects of trigeminal dennervation. To the pest of our knowledge, a detailed description of such a surgical methodology is lacking; reporting of these procedures may facilitate Future research on the trigeminal nerve. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, NEUROSURG SERV, BOSTON, MA 02114 USA. WALSGRAVE GEN HOSP, COVENTRY CV2 2DX, W MIDLANDS, ENGLAND. MIDLAND CTR NEUROSURG & NEUROL, BIRMINGHAM, W MIDLANDS, ENGLAND. NR 19 TC 1 Z9 6 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0270 J9 J NEUROSCI METH JI J. Neurosci. Methods PD APR PY 1996 VL 65 IS 2 BP 137 EP 141 DI 10.1016/0165-0270(95)00129-8 PG 5 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA UJ644 UT WOS:A1996UJ64400002 PM 8740590 ER PT J AU Friedlander, RM Ogilvy, CS AF Friedlander, RM Ogilvy, CS TI Aneurysmal subarachnoid hemorrhage in a patient with bilateral A(1) fenestrations associated with an azygos anterior cerebral artery - Case report and literature review SO JOURNAL OF NEUROSURGERY LA English DT Article DE fenestration; azygos artery; aneurysm; embryology ID INTRACRANIAL SACCULAR ANEURYSMS; COMMUNICATING ARTERY AB Fenestration of the proximal anterior cerebral artery (A(1) segment) is a rare occurrence. This vascular anomaly is often associated with aneurysms and other abnormalities. The current article describes the case of a 33-year-old man who presented with a subarachnoid hemorrhage secondary to a ruptured aneurysm originating from the proximal end of an A, fenestration. This patient also had a contralateral A, fenestration as well as an azygos anterior cerebral artery. This is the first report of such an unusual vascular anatomy. The literature is reviewed and possible embryological mechanisms are discussed. C1 HARVARD UNIV,NEUROSURG SERV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RI Friedlander, Robert/A-2845-2016 OI Friedlander, Robert/0000-0003-4423-9219 NR 33 TC 33 Z9 33 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD APR PY 1996 VL 84 IS 4 BP 681 EP 684 DI 10.3171/jns.1996.84.4.0681 PG 4 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA UC211 UT WOS:A1996UC21100021 PM 8613864 ER PT J AU Henson, JW AF Henson, JW TI Coupling JC virus transcription and replication SO JOURNAL OF NEUROVIROLOGY LA English DT Editorial Material ID BINDING RP Henson, JW (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,SERV NEUROL,149 13TH ST,CHARLESTOWN,MA 02129, USA. FU NINDS NIH HHS [NS 01605] NR 8 TC 2 Z9 2 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 1355-0284 J9 J NEUROVIROL JI J. Neurovirol. PD APR PY 1996 VL 2 IS 2 BP 57 EP 59 DI 10.3109/13550289609146538 PG 3 WC Neurosciences; Virology SC Neurosciences & Neurology; Virology GA UL929 UT WOS:A1996UL92900001 PM 8799196 ER PT J AU Houtman, JJ Fleming, JO AF Houtman, JJ Fleming, JO TI Dissociation of demyelination and viral clearance in congenitally immunodeficient mice infected with murine coronavirus JHM SO JOURNAL OF NEUROVIROLOGY LA English DT Article DE multiple sclerosis; immunopathology; mouse hepatitis virus ID MOUSE HEPATITIS-VIRUS; CENTRAL-NERVOUS-SYSTEM; T-CELL CLONES; MONOCLONAL-ANTIBODIES; INVITRO MODELS; STRAIN JHM; NUDE-MICE; DISEASE; INVIVO; RATS AB Infection of rodents with murine coronavirus JHM results in a subacute or chronic demyelinating disease which serves as a model for the human disease multiple sclerosis. Previous studies with JHMV have established a role for the immune system in both viral clearance and demyelination. To further clarify the role of the immune system in JHMV pathogenesis, several strains of congenitally immunodeficient mice were studied. Infection of immunocompetent C57BL/6 mice with JHMV resulted in severe paralysis and demyelination and complete clearance of infectious virus from the brain (C+D+ phenotype). In contrast, infected SCID mice showed little or no paralysis or demyelination and were unable to clear infectious virus (C-D- phenotype). Athymic nude mice and a proportion of mice lacking MHC Class I or II expression exhibited robust demyelination but did not completely clear infectious virus from the brain (C-D+ phenotype). These results are consistent with an immune-mediated mechanism for JHMV-induced demyelination, but indicate that the immune mechanisms which participate in demyelination and viral clearance are distinct. It may thus be possible to experimentally alter immunopathological responses without impairing antimicrobial immunity. C1 UNIV WISCONSIN, DEPT MED MICROBIOL & IMMUNOL, MADISON, WI 53706 USA. UNIV WISCONSIN, DEPT NEUROL, MADISON, WI 53706 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53705 USA. FU NIGMS NIH HHS [GM07215] NR 52 TC 78 Z9 80 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1355-0284 J9 J NEUROVIROL JI J. Neurovirol. PD APR PY 1996 VL 2 IS 2 BP 101 EP 110 DI 10.3109/13550289609146543 PG 10 WC Neurosciences; Virology SC Neurosciences & Neurology; Virology GA UL929 UT WOS:A1996UL92900006 PM 8799201 ER PT J AU Herbert, V AF Herbert, V TI Introduction SO JOURNAL OF NUTRITION LA English DT Editorial Material ID VITAMIN; DISEASE; MORTALITY; DIETARY C1 BROCKTON W ROXBURY VET AFFAIRS MED CTR,HEMATOL & NUTR RES LAB,RES SERV,BRONX,NY 10468. MT SINAI MED CTR,NEW YORK,NY 10029. MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. RP Herbert, V (reprint author), BRONX VET AFFAIRS MED CTR,MED SERV,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 26 TC 52 Z9 53 U1 0 U2 0 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3166 J9 J NUTR JI J. Nutr. PD APR PY 1996 VL 126 IS 4 SU S BP S1197 EP S1200 PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA UD167 UT WOS:A1996UD16700036 ER PT J AU Kleinman, RE Finberg, LF Klish, WJ Lauer, RN AF Kleinman, RE Finberg, LF Klish, WJ Lauer, RN TI Dietary guidelines for children: US recommendations SO JOURNAL OF NUTRITION LA English DT Article; Proceedings Paper CT 1995 American-Institute-of-Nutrition Annual Meeting CY APR 09-13, 1995 CL ATLANTA, GA SP Amer Inst Nutr DE atherosclerosis; children; cholesterol; fat; growth ID ADULT HYPERCHOLESTEROLEMIA; CHILDHOOD; FAILURE; FAT AB The primary goal for pediatric dietary guidelines is to provide nutrients to support optimal growth and development at different ages from infancy through the end of adolescence. Over the past 15 years increasing attention has been directed toward developing nutrition recommendations that may lower the risk of chronic illness later in life. Recent evidence supports earlier studies that demonstrate that atherogenesis begins in childhood, is an evolving process and is influenced by environmental factors. As a result, in part, because of nutritional recommendations to lower the fat content of the diet, total fat and saturated fat as a percentage of total energy intake have declined in the diet of children and adolescents over the past 20 years. At the same time there has been no increase in the prevalence of growth failure; children, in fact, are heavier than their counterparts of 15 years ago. With a decrease in dietary fat, the mean serum cholesterol of the population as a whole has decreased steadily over the past 20 years. Children can safely eat a lower fat diet in which fat contributes 30% of total energy and saturated fat < 10% of total energy. C1 UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. TEXAS CHILDRENS HOSP,HOUSTON,TX 77030. UNIV IOWA HOSP & CLIN,IOWA CITY,IA 52242. RP Kleinman, RE (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT GASTROINTESTINAL & NUTR UNIT,32 FRUIT ST,VBK 107,BOSTON,MA 02114, USA. NR 21 TC 12 Z9 12 U1 0 U2 0 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3166 J9 J NUTR JI J. Nutr. PD APR PY 1996 VL 126 IS 4 SU S BP S1028 EP S1030 PG 3 WC Nutrition & Dietetics SC Nutrition & Dietetics GA UD167 UT WOS:A1996UD16700007 ER PT J AU Kales, SN Castro, MJ Christiani, DC AF Kales, SN Castro, MJ Christiani, DC TI Epidemiology of hazardous materials responses by Massachusetts district HAZMAT teams SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE LA English DT Article ID CYANIDE; DISASTERS AB Hazardous materials releases can cause substantial morbidity and mortality, but very few studies have systematically investigated them. We analyzed responses by Massachusetts' six district hazardous materials (HAZMAT) teams from the time of their inception through February 1994. Spills, leaks, and other escapes of materials caused or contributed to 67 of 85 (79%) incidents. Transportation-related accidents accounted for 13 of 83 (16%); whereas the remainder of the releases occurred at fixed facilities. The chemicals most frequently involved were various hydrocarbons and corrosive materials. Most incidents (60 of 85 [70%]) had no reported injuries. Civilians were injured in 18 of 85 (21%) incidents; regular fire fighter and/or police were injured in eight of 85 (9%) incidents; and HAZMAT team members in one of 85 incidents (1%). Systematic study is needed to identify preventable causes of HAZMAT responses as well as ideas for batter control of secondary health effects. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM HLTH,OCCUPAT HLTH PROGRAM,BOSTON,MA 02115. NEWTON FIRE DEPT,NEWTON,MA. METROFIRE HAZ MAT TEAM,NEWTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PULM CRIT CARE UNIT,BOSTON,MA 02114. MASSACHUSETTS RESP HOSP,CTR OCCUPAT & ENVIRONM MED,BRAINTREE,MA 02184. RP Kales, SN (reprint author), HARVARD UNIV,CAMBRIDGE HOSP,SCH MED,DEPT MED,1493 CAMBRIDGE ST,CAMBRIDGE,MA 02139, USA. FU NIEHS NIH HHS [ES00002, ES05947] NR 29 TC 14 Z9 14 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1076-2752 J9 J OCCUP ENVIRON MED JI J. Occup. Environ. Med. PD APR PY 1996 VL 38 IS 4 BP 394 EP 400 DI 10.1097/00043764-199604000-00018 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA UF039 UT WOS:A1996UF03900014 PM 8925324 ER PT J AU Tanner, A Kent, R Maiden, MFJ Taubman, MA AF Tanner, A Kent, R Maiden, MFJ Taubman, MA TI Clinical, microbiological and immunological profile of healthy, gingivitis and putative active periodontal subjects SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Article DE gingivitis; periodontitis; microbiology; immunology ID ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; BACTEROIDES-INTERMEDIUS; ATTACHMENT LEVEL; BACTERIOLOGY; DISEASES; MICROBIOTA; LESIONS; MICROORGANISMS; PROGRESSION; ANTIBODIES AB Thirteen periodontally healthy subjects were monitored clinically for 6-12 months. Clinical measurements at g-weekly intervals included duplicate PD measurements, presence of plaque, redness, and bleeding on probing. Baseline measurements consisted of 2 visits 1 wk apart. Microbial samples were taken from 11 of the subjects who had completed at least 8 months of monitoring. Levels of serum antibodies to 12 periodontal species were determined from 10 subjects. Standard deviations of replicate PD measurements, computed for each subject, ranged from 0.2-0.3 mm over the monitoring period. Plaque and redness increased during monitoring, and showed a weak association with PD change. Baseline and follow-up distributions of PD changes indicated that changes of >1.5 mm could reasonably be considered to represent active sites. Five subjects demonstrated at least 1 site deepening by 1.5 mm over the period monitored, and these were considered putative active subjects. Sites from 2 subjects showed PD increases in the 6 wk just before sampling, and these were considered to represent active sites. Species associated with putative active subjects included Actinomyces naeslundii, Veillonella parvula, Selenomonas noxia and Prevotella nigrescens. Streptococcus sanguis, S. gordonii and Peptostreptococcus micros were associated with inactive subjects. S. gordonii and S. oralis were associated with health, whereas P. nigrescens was associated with gingivitis. Elevated serum antibodies were detected to A. actinomycetemcomitans in 4 subjects. The predominant microbiota of putative active subjects included some species previously associated with gingivitis, and some species previously associated with progressing periodontitis. RP Tanner, A (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-03488, DE-03420, DE-09513] NR 32 TC 51 Z9 51 U1 0 U2 3 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD APR PY 1996 VL 31 IS 3 BP 195 EP 204 DI 10.1111/j.1600-0765.1996.tb00484.x PG 10 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA UU313 UT WOS:A1996UU31300007 PM 8814590 ER PT J AU Strack, S AF Strack, S TI Introduction to the special series - Interpersonal theory and the interpersonal circumplex: Timothy Leary's legacy SO JOURNAL OF PERSONALITY ASSESSMENT LA English DT Editorial Material ID INVENTORY; TAXONOMY; SCALES RP Strack, S (reprint author), US DEPT VET AFFAIRS,OUTPATIENT CLIN,PSYCHOL SERV 116B,351 E TEMPLE ST,LOS ANGELES,CA 90012, USA. NR 23 TC 4 Z9 5 U1 0 U2 2 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0022-3891 J9 J PERS ASSESS JI J. Pers. Assess. PD APR PY 1996 VL 66 IS 2 BP 212 EP 216 DI 10.1207/s15327752jpa6602_1 PG 5 WC Psychology, Clinical; Psychology, Social SC Psychology GA UB249 UT WOS:A1996UB24900002 PM 16367699 ER PT J AU Fei, HL Frame, LH AF Fei, HL Frame, LH TI d-Sotalol terminates reentry by two mechanisms with different dependence on the duration of the excitable gap SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID III ANTIARRHYTHMIC AGENTS; ACTION-POTENTIAL DURATION; CANINE ATRIAL-FLUTTER; VENTRICULAR TACHYARRHYTHMIAS; CARDIAC-MUSCLE; TRICUSPID RING; REFRACTORINESS; ARRHYTHMIAS; INVITRO; MODEL AB We used eight adjustable preparations in which the canine atrial tricuspid rings were cut and reconnected electronically by sensing activation on one side of the cut and pacing the other after an adjustable delay. A long delay resulted in a long cycle length (CL) and excitable gap (EG) during reentry. Decreasing delay decreased CL and EG. d-Sotalol (4 mg/l) significantly increased effective refractory period (ERP) and action potential duration with no effects on conduction time during constant 400-msec pacing. During reentry, d-sotalol increased action potential durations more than CLs, so it decreased diastolic intervals. It decreased EG by increasing ERP more than CL. Although d-sotalol increased action potential duration more at longer delays with longer CLs, showing reverse use-dependence, it terminated sustained tachycardias by increasing ERP only for the short delays when the initial EG was short. In 5 of 8 experiments, longer equilibration with d-sotalol produced fixed block at a vulnerable site, so reentry could not be induced at any delays. Fixed block could be transiently reversed by ACh and resolved after washout of d-sotalol. We conclude that d-sotalol terminated reentry by two mechanisms: 1) It terminated sustained reentry by increasing ERP when the initial EG was sufficiently short. 2) In some preparations, it caused fixed block at a vulnerable site, which prevented reentry regardless of the initial EG. C1 VET AFFAIRS MED CTR,CARDIOL SECT 111C,PHILADELPHIA,PA 19104. UNIV PENN,DEPT MED,DIV CARDIOVASC,PHILADELPHIA,PA 19104. FU NHLBI NIH HHS [HL38386] NR 43 TC 10 Z9 10 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD APR PY 1996 VL 277 IS 1 BP 174 EP 185 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UE585 UT WOS:A1996UE58500024 PM 8613916 ER PT J AU Goodman, A Hutchinson, ML AF Goodman, A Hutchinson, ML TI Cell surplus on sampling devices after routine cervical cytologic smears - A study of residual cell populations SO JOURNAL OF REPRODUCTIVE MEDICINE LA English DT Article DE cervical smears; sampling studies AB OBJECTIVE: To demonstrate whether considerable valuable cellular material remains on the sampling device after a conventional cervical cytologic smear and to investigate whether evidence of cervical disease may be present on the sampling device but missed because it is not represented on the first slide. STUDY DESIGN: Routine cervical cytologic smear material was taken from 60 women who were attending the colposcopy or gynecologic oncology clinic at New England Medical Center. At the time of the colposcopic examination, a cervical scrape was made using a Cytobrush followed by a Cervex brush. After the smear was made from each device, the sampling devices were used to make four additional slides. Both the Cytobrush and Cervex brush were applied to each slide. RESULTS: Cytologically, all five slides were satisfactory for screening in the 60 cases. In all diagnostic cases but one, disease was well represented across all five slides. CONCLUSIONS: Cellular material collected in a cervical scrape is sufficient to prepare at least five satisfactory smears. The one case where an abnormality was detected only on the third slide suggests the possibility of nonrandom subsampling and of discarding the majority of the cellular material from the patient. C1 TUFTS UNIV NEW ENGLAND MED CTR,DEPT PATHOL,BOSTON,MA 02111. RP Goodman, A (reprint author), MASSACHUSETTS GEN HOSP,DEPT GYNECOL,DIV GYNECOL ONCOL,55 FRUIT ST,BOSTON,MA 02114, USA. NR 10 TC 22 Z9 22 U1 0 U2 0 PU SCI PRINTERS & PUBL INC PI ST LOUIS PA P.O. DRAWER 12425 8342 OLIVE BLVD, ST LOUIS, MO 63132 SN 0024-7758 J9 J REPROD MED JI J. Reprod. Med. PD APR PY 1996 VL 41 IS 4 BP 239 EP 241 PG 3 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA UF707 UT WOS:A1996UF70700006 PM 8728075 ER PT J AU Polisson, RP Gilkeson, GS Pyun, EH Pisetsky, DS Smith, EA Simon, LS AF Polisson, RP Gilkeson, GS Pyun, EH Pisetsky, DS Smith, EA Simon, LS TI A multicenter trial of recombinant human interferon gamma in patients with systemic sclerosis, effects on cutaneous fibrosis and interleukin 2 receptor levels SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE interferon gamma; scleroderma; progressive systemic sclerosis; Raynaud's phenomenon; interleukin-2 receptor ID FIBROBLAST COLLAGEN-SYNTHESIS; PROCOLLAGEN MESSENGER-RNA; SCLERODERMA SKIN; INHIBITION; EXPRESSION; MOUSE; CELLS AB Objective. To evaluate the acute toxicity, potential efficacy, and effects on the soluble interleukin 2 receptor (sIL-2R) of recombinant human interferon gamma (rIFN-gamma) in patients with systemic sclerosis (SSc). Methods. A multicentered, pilot clinical trial of rIFN-gamma was performed on 20 patients (15 women, 5 men, mean age 45 years) with active cutaneous Sc (mean disease duration 36 months) to evaluate its potential as a novel therapy for this untreatable disorder. After one week of rIFN-gamma 0.01 mg/m(2)/day, subjects self-administered rIFN-gamma 0.1 mg/m(2)/day intramuscularly for a total of 18 weeks. The major outcome variable was a modified skin score (0 = normal skin, 3 = hidebound skin) measured and summed from 15 anatomic areas of the body, sIL-2R levels were measured by ELISA at entry and exit from the study. Results. The clinical results were modest at best. Nine of 20 patients achieved at least a 20% reduction in skin score, with one patient showing almost total remission of all skin abnormalities. The mean skin score at entry for all subjects was 22.8 +/- 8.9 and over the course of the trial improved marginally compared to baseline (mean change -4.72 +/- 6.62; p = 0.008). However, 8 subjects did not change appreciably while in the trial, Antibodies to Scl-70 were observed in only 5 patients (all with diffuse scleroderma) and were not associated with either response to or complications from therapy, The adverse reactions were frequent and occasionally severe. Ten subjects were withdrawn because of exacerbation of Raynaud's symptoms (n = 5), constitutional symptoms (n = 2), development of renal crises (n = 2), aand mild pancytopenia (n = 1). Minor laboratory abnormalities were common and included elevation of cholesterol, triglycerides, hepatic transaminases, and reduction in white blood cell count. Compared to controls, mean sIL-2R was markedly elevated at entry (1309 +/- 495 U/ml; p = 0.0001) and did not change appreciably at exit. Spearman correlation analysis showed a trend but no statistically significant association of skin score with sn-2R (R = 0.408; p = 0.074), However, sIL-2R was significantly correlated with erythrocyte sedimentation rate (R = 0.542; p = 0.0165), A subset analysis revealed that skin score (p = 0.0001) and sIL-2R (p = 0.00170) were significantly higher at baseline for patients with diffuse scleroderma compared to patients with limited disease. Conclusion. rIFN-gamma may be beneficial for some patients with SSc, but the benefit appears marginal for most individuals and the side effects frequent. Although sIL-2R was elevated in many of the patients with SSc, it did not appear to be correlated with activity of cutaneous disease or response to therapy. C1 DUKE UNIV,MED CTR,DIV RHEUMATOL & IMMUNOL,DURHAM,NC. VET ADM MED CTR,DURHAM,NC. MED UNIV S CAROLINA,DEPT MED,DIV RHEUMATOL & IMMUNOL,CHARLESTON,SC 29425. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT MED,RHEUMATOL SECT,BOSTON,MA 02215. RP Polisson, RP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ARTHRIT UNIT,MED SERV,BULFINCH 1,BOSTON,MA 02114, USA. NR 21 TC 59 Z9 59 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD APR PY 1996 VL 23 IS 4 BP 654 EP 658 PG 5 WC Rheumatology SC Rheumatology GA UE520 UT WOS:A1996UE52000016 PM 8730122 ER PT J AU Bunting, RW Selig, MK Dickersin, GR AF Bunting, RW Selig, MK Dickersin, GR TI Ultrastructure of peripheral blood granulocytes from patients with low serum cobalamin SO JOURNAL OF SUBMICROSCOPIC CYTOLOGY AND PATHOLOGY LA English DT Article DE cobalamin deficiency; peripheral blood ultrastructure ID CHROMOSOME-16; ASSOCIATION; LEUKEMIA AB Peripheral blood granulocytes from ten patients with low serum cobalamin were studied using light and electron microscopic techniques. Six patients had classic neutrophil hypersegmentation using light microscopy, bur three patients had an increase in band forms and rare hypersegmented cells. The electron microscope revealed nuclear appendages consisting of nuclear stalks, rings and blebs in neutrophils from all patients regardless of the degree of hypersegmentation but not from normal controls; these did not appear to result from sectioning artifact and their formation may be interrelated. Numerous cytoplasmic empty granules were seen in neutrophils from three patients. Another three showed what appeared to be granules in the shape of water-wings under low power, bur on higher power were unique mitochondria. Some disorder of the eosinophil granule centrum was seen in all patients but was extreme in four patients; lipid cytoplasmic inclusions were also seen in these four and one other patient. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. RP Bunting, RW (reprint author), SPAULDING REHABIL HOSP,DEPT HEMATOL,125 NASHUA ST,BOSTON,MA 02114, USA. NR 36 TC 6 Z9 6 U1 0 U2 0 PU EDITRICE COMPOSITORI BOLOGNA PI BOLOGNA PA VIA STALINGRADO 97/2, I-40128 BOLOGNA, ITALY SN 1122-9497 J9 J SUBMICR CYTOL PATH JI J. Submicrosc. Cytol. Pathol. PD APR PY 1996 VL 28 IS 2 BP 187 EP 195 PG 9 WC Pathology SC Pathology GA UJ393 UT WOS:A1996UJ39300006 PM 8964043 ER PT J AU Ruka, W Taghian, A Gioioso, D Fletcher, JA Preffer, F Suit, HD AF Ruka, W Taghian, A Gioioso, D Fletcher, JA Preffer, F Suit, HD TI Comparison between the in vitro intrinsic radiation sensitivity of human soft tissue sarcoma and breast cancer cell lines SO JOURNAL OF SURGICAL ONCOLOGY LA English DT Article DE intrinsic radiation sensitivity; SF2; mean inactivation dose; soft tissue sarcomas; breast carcinoma cell lines ID HUMAN-TUMOR CELLS; SURVIVAL CURVES; RADIOBIOLOGICAL CHARACTERIZATION; MULTICELLULAR SPHEROIDS; INITIAL SLOPE; LOCAL-CONTROL; RADIOSENSITIVITY; RADIOTHERAPY; INVITRO; RECURRENCE AB The purpose of this study is to evaluate the radiation sensitivity of human soft tissue sarcoma cell lines in vitro and to compare with that of human breast carcinoma and glioblastoma cell lines. The intrinsic radiation sensitivity parameters of seven human soft tissue sarcomas and eight breast carcinoma cell lines were investigated in vitro by clonogenic assays for single-dose irradiation under aerobic conditions on cells in exponential phase of growth. The results for sarcoma cell lines showed that the mean surviving fraction at 2 Gy (SF2) was 0.39 (SD +/- 0.09) with a range of 0.24 to 0.53, and the average mean inactivation dose (MID) was 1.92 (SD +/- 0.35) range from 1.36 Gy to 2.49 Gy. These values were not different from that of breast cell lines examined concurrently and using the same experimental methods (mean SF2 0.38, SD +/- 0.09; MID 1.9 Gy, SD +/- 0.37). However, radiobiological parameters of nine karyotyped human malignant glioma cell lines determined earlier in this laboratory were significantly higher (mean SF2 0.50 +/- 0.14; mean MID 2.61 +/- 0.60). In conclusion, the data presented here do not support the view that cells of sarcomas show unusual radiation resistance. To the extent that the in vitro determined cellular radiation sensitivity reflects the tumor response in vivo, the success rate for radiation applied against sarcoma and breast carcinoma of comparable size could be similar. (C) 1996 Wiley-Liss, Inc. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB RADIAT BIOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,FLOW CYTOMETRY LAB,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT PATHOL,CYTOGENET LAB,BOSTON,MA 02115. FU NCI NIH HHS [CA13311] NR 28 TC 12 Z9 12 U1 0 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0022-4790 J9 J SURG ONCOL JI J. Surg. Oncol. PD APR PY 1996 VL 61 IS 4 BP 290 EP 294 DI 10.1002/(SICI)1096-9098(199604)61:4<290::AID-JSO13>3.0.CO;2-A PG 5 WC Oncology; Surgery SC Oncology; Surgery GA UF425 UT WOS:A1996UF42500013 PM 8628001 ER PT J AU Wolfort, SF Reiken, SR Berthiaume, F Tompkins, RG Yarmush, ML AF Wolfort, SF Reiken, SR Berthiaume, F Tompkins, RG Yarmush, ML TI Control of hypertrophic scar growth using antibody-targeted photolysis SO JOURNAL OF SURGICAL RESEARCH LA English DT Article ID INTERFERON-GAMMA; KELOIDS; EXPRESSION; MICE AB Hypertrophic scar is marked by excess collagen accumulation secondary to an increased vascularization response in the scar and an increase in fibroblast cell density. It is currently the most debilitating longterm complication of the surviving burn patient, and at present, there is no routinely effective form of therapy. In this study, we investigated the potential use of antibody-targeted photolysis (ATPL) in treating hypertrophic scars. An immunoconjugate consisting of a photosensitizer (Sn-chlorin e6) linked to a monoclonal antibody that binds to human myofibroblasts (PR2D3) was prepared, which in response to photoactivation produces singlet oxygen in close proximity to the target cell surface. The model used for these studies consisted of 1-mm(3) human hypertrophic scar tissue implants in athymic mice, These implants increase approximately 20-fold in volume over a period of 15 days. Four days after implantation immunoconjugate was injected directly into scar implants and allowed to diffuse throughout for 24 hr before implants were illuminated with laser light at 630 nm (120 J/cm(2)), ATPL treatment caused a significant reduction in total growth compared to the untreated controls (P < 0.05). No effect was observed when an irrelevant conjugate (anti-Pseudomonas aeruginosa) was used. Histological examination of the ATPL-treated implants 24 hr post-ATPL revealed the presence of a large number of lipid droplets indicative of massive cell damage and infiltration by mononuclear cells and neutrophils. (C) 1996 Academic Press, Inc. C1 SHRINERS BURNS INST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA 02114. FU NIGMS NIH HHS [T32-GM07350] NR 23 TC 15 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD APR PY 1996 VL 62 IS 1 BP 17 EP 22 DI 10.1006/jsre.1996.0166 PG 6 WC Surgery SC Surgery GA UF249 UT WOS:A1996UF24900004 PM 8606503 ER PT J AU Vacanti, FX Kwun, BD AF Vacanti, FX Kwun, BD TI Vascular occlusion produced over 24 hours increases spinal cord tolerance to occlusion SO JOURNAL OF SURGICAL RESEARCH LA English DT Article ID AORTIC-ANEURYSMS; CNS ISCHEMIA; CELL-DEATH; HYPOTHERMIA; CHANNEL; PROTECT; DAMAGE; MODEL AB Occlusion over a 24-hr period of vessels which supply the spinal cord was tolerated better than occlusion of the same vessels acutely, Spinal cord ischemia was produced in 12 New Zealand White rabbits by transection of four of five pairs of lumbar segmental arteries arising from the abdominal aorta plus 30-min occlusion of the remaining segmental artery pair either acutely or 24 hr later. Of these 12 rabbits, 6 were occluded acutely and served as controls, Recovery, or failure to recover, as assessed by examining the rabbits for permanent loss of sensory and motor function in the hindlimbs, was compared in the two groups, The duration of the temporary occlusion was sufficient to lead to a total or near total loss of sensory and motor function in all control rabbits but resulted in no deficit in all but 1 of the rabbits which had the occlusion produced in two stages, These results have implications for the care of patients subjected to spinal cord ischemia during and after operations on the thoracic aorta. (C) 1996 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. RP Vacanti, FX (reprint author), MASSACHUSETTS GEN HOSP,ANESTHESIA SERV,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL 22573] NR 20 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD APR PY 1996 VL 62 IS 1 BP 29 EP 31 DI 10.1006/jsre.1996.0168 PG 3 WC Surgery SC Surgery GA UF249 UT WOS:A1996UF24900006 PM 8606505 ER PT J AU Vacanti, FX Kwun, BD AF Vacanti, FX Kwun, BD TI Carbon dioxide at anesthetic levels protects against irreversible damage during spinal cord ischemia SO JOURNAL OF SURGICAL RESEARCH LA English DT Article ID CNS ISCHEMIA; AORTIC-ANEURYSMS; CELL-DEATH; CHANNEL; PH AB Carbon dioxide inspired as a 40% mixture in oxygen and halothane protected the spinal cords of 5 rabbits subjected to 30 min of surgically created spinal cord ischemia. Spinal cord ischemia was produced in 20 New Zealand White rabbits by transection of four of the five pairs of segmental arteries arising from the abdominal aorta below the renal arteries plus temporary occlusion of the remaining pair, The artery was occluded for 15 min in 9 control rabbits, for 30 min in 6 control rabbits, and for 30 min in 5 treated rabbits after inhalation of 40% carbon dioxide. The extent of spinal cord injury was assessed by examining the rabbits for permanent loss of sensory and motor function in the hindlimbs and was compared in the treated and control groups. These results have implications for the management of patients subjected to aortic occlusion. (C) 1996 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. RP Vacanti, FX (reprint author), MASSACHUSETTS GEN HOSP,ANESTHESIA SERV,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL 22573] NR 24 TC 2 Z9 3 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD APR PY 1996 VL 62 IS 1 BP 59 EP 62 DI 10.1006/jsre.1996.0173 PG 4 WC Surgery SC Surgery GA UF249 UT WOS:A1996UF24900011 PM 8606511 ER PT J AU Kelly, OE Johnson, DH Delgutte, B Cariani, P AF Kelly, OE Johnson, DH Delgutte, B Cariani, P TI Fractal noise strength in auditory-nerve fiber recordings SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Article ID NEURAL SPIKE TRAIN; DISCHARGE; MODEL; TRANSDUCTION; CAT; SIMULATION; RECEPTOR AB Discharge patterns recorded from single auditory-nerve fibers have demonstrated long-range dependence, with the count variance-to-mean ratio growing as a power of the counting time for times greater than 0.1-1 s. The intent of this study is-to provide a large dataset to enable a more detailed investigation of this phenomenon. Based on 108 recordings from a cat, we conclude that the presence of the fractal noise in the discharge rate is : Independent of characteristic frequency and stimulus level, but does depend on discharge rate. We measured the low-frequency power of the fractal noise, finding its coefficient of variation to range between 6% and 26% and to decrease as firing rate increases. Such behavior is consistent with multiplicative fractal variations in models of the hair cell membrane permeability to neurotransmitter. Measured standard deviations of spike rate correspond to a sound-pressure level difference limen of approximately 1 dB. (C) 1996 Acoustical Society of America. C1 MASSACHUSETTS EYE & EAR INFIRM, EATON PEABODY LAB, BOSTON, MA 02114 USA. RP Kelly, OE (reprint author), RICE UNIV, DEPT ELECT & COMP ENGN, COMP & INFORMAT TECHNOL INST, MS366, 6100 MAIN ST, HOUSTON, TX 77005 USA. FU NIDCD NIH HHS [DC00019]; NIMH NIH HHS [MH46453] NR 35 TC 19 Z9 20 U1 0 U2 2 PU ACOUSTICAL SOC AMER AMER INST PHYSICS PI MELVILLE PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA SN 0001-4966 J9 J ACOUST SOC AM JI J. Acoust. Soc. Am. PD APR PY 1996 VL 99 IS 4 BP 2210 EP 2220 DI 10.1121/1.415409 PN 1 PG 11 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA UF398 UT WOS:A1996UF39800048 PM 8730068 ER PT J AU Lees, S Hanson, DB Page, EA AF Lees, S Hanson, DB Page, EA TI Some acoustical properties of the otic bones of a fin whale SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Article AB The otic bones in this report are the tympanic bulla, the periotic, and the three ossicles (malleus, incus, and stapes) of an adult fin whale (Balaenoptera physalus). The purpose was to determine if the periotic was denser than the other otic bones. It was found in one male adult fin whale that the density of all the otic bones is approximately the same, 2.50 kg/m(3) with a maximum of 2.58. The lowest density was observed in the stapes (2.36). The sonic velocity seems to vary as the density but there also seems to be a structural effect. The maximum sonic velocity was 4.89 km/s in the malleus. The specific acoustic impedance was as high as 12.5 megarayles in the periotic. These values compare with those for human femur of 1.95 for the density, 3.73 for the sonic velocity, and 7.33 for the specific acoustic impedance. The ossicles weigh as much as 200 times as much as human ossicles. The density of whale ossicles are about ten percent greater than human ossicles. The mechanical natural frequency of the whale ossicles must be very low. The approximate uniformity of the properties of this whale's otic bones may be characteristic of the middle ear. The density of the otic bones of land mammals is less than for whales. The density of the horse petrosal (2.29 g/cc) is essentially the same as the density of adult human ossicles (2.23-2.27 g/cc). The high density of the otic bones for all mammals suggests it may be related to hearing acuity perhaps by increasing the specific acoustic impedance, which increases the acoustic contrast with the other body tissues. (C) 1996 Acoustical Society of America. RP Lees, S (reprint author), FORSYTH DENT CTR,DEPT BIOENGN,140 FENWAY,BOSTON,MA 02115, USA. NR 6 TC 10 Z9 10 U1 0 U2 1 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0001-4966 J9 J ACOUST SOC AM JI J. Acoust. Soc. Am. PD APR PY 1996 VL 99 IS 4 BP 2421 EP 2427 DI 10.1121/1.415430 PN 1 PG 7 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA UF398 UT WOS:A1996UF39800069 ER PT J AU Spencer, T Biederman, J Wilens, T Harding, M ODonnell, BAD Griffin, S AF Spencer, T Biederman, J Wilens, T Harding, M ODonnell, BAD Griffin, S TI Pharmacotherapy of attention-deficit hyperactivity disorder across the life cycle SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Review DE attention-deficit hyperactivity disorder; psychopharmacology; comorbidity ID MINIMAL BRAIN-DYSFUNCTION; AGGRESSIVE NONCOMPLIANT FEATURES; NERVOUS-SYSTEM STIMULANTS; MOTHER-CHILD INTERACTIONS; LA-TOURETTES SYNDROME; DOUBLE-BLIND; PSYCHIATRIC STATUS; RESIDUAL TYPE; METHYLPHENIDATE TREATMENT; HYPERKINETIC CHILDREN AB Objective: To evaluate the scope of the available therapeutic armamentarium in attention-deficit hyperactivity disorder (ADHD). Method: The literature of medication trials in ADHD was systematically reviewed, with attention to issues of psychiatric comorbidity, age, gender, and ethnic background. Results: One hundred fifty-five controlled studies of 5,768 children, adolescents, and adults have documented the efficacy of stimulants in an estimated 70% of subjects. The literature clearly documents that stimulants not only improve abnormal behaviors of ADHD, but also self-esteem, cognition, and social and family function. However, response varied in different age groups and with certain comorbid conditions. In addition, there is an impressive body of literature documenting the efficacy of tricyclic antidepressants on ADHD in more than 1,000 subjects. Studies of alternative antidepressants, antipsychotics, antihypertensives, and other compounds were also reviewed. Conclusions: The available literature indicates the important role of psychopharmacological agents in the reduction of the core symptoms of ADHD and associated impairments. More research is needed on alternative pharmacological treatments and to further evaluate established therapeutics beyond school-age Caucasian boys. In addition, more research is needed on the efficacy of treatment for comorbid ADHD, use of combined medications, and the combination of medication and psychosocial treatment. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP Spencer, T (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,WACC 725,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 201 TC 491 Z9 503 U1 15 U2 85 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD APR PY 1996 VL 35 IS 4 BP 409 EP 432 DI 10.1097/00004583-199604000-00008 PG 24 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA UB759 UT WOS:A1996UB75900008 PM 8919704 ER PT J AU Ablon, SL AF Ablon, SL TI The therapeutic action of play SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP Ablon, SL (reprint author), MASSACHUSETTS GEN HOSP,ACC 725,FRUIT ST,BOSTON,MA 02114, USA. NR 7 TC 13 Z9 13 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD APR PY 1996 VL 35 IS 4 BP 545 EP 547 PG 3 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA UB759 UT WOS:A1996UB75900022 PM 8919718 ER PT J AU Bigby, M Gadenne, AS AF Bigby, M Gadenne, AS TI Understanding and evaluating clinical trials SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Review ID HAIRY-CELL LEUKEMIA; ADVERSE DRUG-REACTIONS; RECOMBINANT ALPHA-2 INTERFERON; ADDITIONAL BASIC SCIENCE; RANDOMIZED CONTROL TRIAL; MEDICAL LITERATURE; SAMPLE-SIZE; OPERATIONAL ASSESSMENT; LINE COMPARISONS; USERS GUIDES AB In this review, we attempt to provide the basic knowledge necessary to understand and evaluate clinical trials because properly conducted, randomized clinical trials are the best sources for determining the best available treatment. Other commonly used sources rarely provide sufficient detail necessary to determine the efficacy and safety of any treatment, and they often contain biases or pitfalls that make them unacceptable or unreliable. Our method for reviewing clinical trials allows a busy clinician to use his or her time most efficiently by deciding not to read the majority of poorly conceived, designed, executed, or reported trials and those trials with insignificant results. It provides a means to determine the quality of the trials that one does decide to read and to retain and retrieve the information when it is needed. The method involves recognizing and evaluating the features that strengthen clinical trials and help validate their conclusions. These features include proper selection and allocation of patients, inclusion of an appropriate control group, randomization, prior selection of clinically and biologically important outcome variables, blinding of assessment, consideration of patient compliance and drop out, and proper presentation and statistical analysis of results. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. BETH ISRAEL HOSP,BOSTON,MA 02215. UNIV CINCINNATI,DEPT DERMATOL,CINCINNATI,OH 45221. RP Bigby, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114, USA. NR 168 TC 44 Z9 45 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD APR PY 1996 VL 34 IS 4 BP 555 EP 590 DI 10.1016/S0190-9622(96)80053-3 PG 36 WC Dermatology SC Dermatology GA UC798 UT WOS:A1996UC79800001 PM 8601646 ER PT J AU Grevelink, JM Duke, D vanLeeuwen, RL Gonzalez, E DeCoste, SD Anderson, RR AF Grevelink, JM Duke, D vanLeeuwen, RL Gonzalez, E DeCoste, SD Anderson, RR TI Laser treatment of tattoos in darkly pigmented patients: Efficacy and side effects SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID Q-SWITCHED RUBY; DOSE-RESPONSE; NM AB Background: Many modalities for the treatment of tattoos and pigmented lesions produce a greater risk of complications in Fitzpatrick types V and VI skin because of an increased incidence of adverse pigmentary changes and keloidal scarring. In fair-skinned persons, Q-switched lasers have proved effective in removing pigmented lesions and tattoos without scarring. Objective: This study was conducted to determine the efficacy and effects of Q-switched lasers on a small series of darkly pigmented patients with tattoos. Methods: Four patients of Ethiopian origin with facial and neck tribal tattoos were treated with both the Q-switched ruby and Nd:YAG lasers. One black woman with a multicolored tattoo on the mid chest was treated with the Q-switched ruby laser. Results: Clearing of all lesions was seen. The treatments did not result in scarring or permanent pigment changes other than the ones intended. Conclusion: Our results indicate that in darkly pigmented patients, Q-switched laser treatment of tattoos can be performed successfully. The longer wavelength Q-switched Nd:YAG laser is recommended when removing tattoos in darker complected persons. A test treatment is advised before treatment of large skin areas. RP Grevelink, JM (reprint author), MASSACHUSETTS GEN HOSP,DERMATOL LASER CTR,275 CAMBRIDGE ST,SUITE 503,BOSTON,MA 02114, USA. NR 14 TC 50 Z9 51 U1 0 U2 2 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD APR PY 1996 VL 34 IS 4 BP 653 EP 656 DI 10.1016/S0190-9622(96)80068-5 PG 4 WC Dermatology SC Dermatology GA UC798 UT WOS:A1996UC79800011 PM 8601656 ER PT J AU Kassan, DG Lynch, AM Stiller, MJ AF Kassan, DG Lynch, AM Stiller, MJ TI Physical enhancement of dermatologic drug delivery: Iontophoresis and phonophoresis SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Review ID TAP WATER IONTOPHORESIS; LOCAL-ANESTHESIA; HYDROCORTISONE PHONOPHORESIS; TRANSDERMAL DELIVERY; LIDOCAINE ANESTHESIA; MOUSE SKIN; HYPERHIDROSIS; ULTRASOUND; THERAPY; INVIVO AB Iontophoresis and phonophoresis are emerging technologies capable of enhancing drug penetration through the stratum corneum, the principal barrier to percutaneous absorption. With utilization of applied electric current or ultrasonic waves, respectively, iontophoresis and phonophoresis have shown efficacy in an increasing number of clinical applications. This article reviews the underlying principles, current status, and potential of iontophoresis and phonophoresis in dermatologic therapy. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT DERMATOL,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02114. MT SINAI SCH MED,DEPT DERMATOL,BOSTON,MA. NR 76 TC 53 Z9 55 U1 0 U2 5 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD APR PY 1996 VL 34 IS 4 BP 657 EP 666 DI 10.1016/S0190-9622(96)80069-7 PG 10 WC Dermatology SC Dermatology GA UC798 UT WOS:A1996UC79800012 PM 8601657 ER PT J AU Rodriguez, A Mele, E Peyregne, E Bullon, F PerezBalino, N Liprandi, MIS Palacios, IF AF Rodriguez, A Mele, E Peyregne, E Bullon, F PerezBalino, N Liprandi, MIS Palacios, IF TI Three-year follow-up of the Argentine randomized trial of percutaneous transluminal coronary angioplasty versus coronary artery bypass surgery in multivessel disease (ERACI) SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID UNSTABLE ANGINA; COMPLETE REVASCULARIZATION; DIRECTIONAL ATHERECTOMY; CONSECUTIVE PATIENTS; IMMEDIATE AB Objectives. The purpose of this study was to report the 3-year follow up results of the ERACI trial (Argentine Randomized Trial of Percutaneous Transluminal Coronary Angioplasty Versus Coronary Artery Bypass Surgery in Multivessel Disease). Background. Although coronary angioplasty has been used with increased frequency in patients with multivessel coronary artery disease, its value, compared with bypass graft surgery, has not been established, Thus, controlled, randomized clinical trials such as the ERACI are needed. Methods. In this trial 127 patients who had multivessel coronary artery disease and clinical indication of myocardial revascularization were randomized to undergo coronary angioplasty (n = 63) or bypass surgery (n = 64). The primary end point of this study was event-free survival (survival with freedom from myocardial infarction, angina and new revascularization procedures) for both groups of patients at 1, 3 and 5 years of follow up. Results. Freedom from combined cardiac events (death, Q-wave myocardial infarction, angina and repeat revascularization procedures) was significantly greater for the bypass surgery group than the coronary angioplasty group (77% vs. 47%; p < 0.001). There were no differences in overall (4.7% vs. 9.5%; p = 0.5) and cardiac (4.7% vs. 4.7%; p = 1) mortality or in the frequency of myocardial infarction (7.8% vs. 7.8%; p = 0.8) between the two groups. However, patients who had bypass surgery were more frequently free of angina (79% vs. 57%; p < 0.001) and required fewer additional reinterventions (6.3% vs, 37%; p < 0.001) than patients who had coronary angioplasty, Conclusions. 1) Freedom from combined cardiac events at 3-year follow-up was greater in patients who had bypass surgery than in those who had coronary angioplasty. 2) The coronary angioplasty group had a higher incidence of recurrence of angina and the need for repeat revascularization procedures. 3) Cumulative cost at 3-year follow-up was greater for the bypass surgery group than for the coronary angioplasty group. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. ANCHORENA HOSP,CARDIAC UNIT,BUENOS AIRES,DF,ARGENTINA. NR 33 TC 74 Z9 76 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1996 VL 27 IS 5 BP 1178 EP 1184 DI 10.1016/0735-1097(95)00592-7 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA UD651 UT WOS:A1996UD65100029 PM 8609339 ER PT J AU Padial, LR Freitas, N Sagie, A Newell, JB Weyman, AE Levine, RA Palacios, IF AF Padial, LR Freitas, N Sagie, A Newell, JB Weyman, AE Levine, RA Palacios, IF TI Echocardiography can predict which patients will develop severe mitral regurgitation after percutaneous mitral valvulotomy SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID BALLOON VALVULOPLASTY; VALVE AREA; VALVOTOMY; STENOSIS; MECHANISMS; DOPPLER; COMMISSUROTOMY; DILATATION; INCREASE; ADULTS AB Objectives. Using two-dimensional echocardiography, we sought to identify features that are associated with severe mitral regurgitation after percutaneous mitral valvulotomy and combine them into a predictive score. Background. Severe mitral regurgitation after percutaneous mitral valvulotomy is a major complication carrying an adverse prognosis that, to date, has not been predictable in advance. Methods. In a consecutive series of 566 patients who underwent percutaneous mitral valvulotomy, 37 (6.5%) developed severe mitral regurgitation (assessed by angiography) after the procedure, 31 of whom had an echocardiogram available before percutaneous mitral valvulotomy. These 31 patients were matched by age, gender, mitral valve area and degree of mitral regurgitation before valvulotomy with 31 randomly selected patients who did not develop severe mitral regurgitation after percutaneous mitral valvulotomy. An echocardiographic score was developed on the basis of the pathologic studies of valves of patients who developed severe regurgitation after percutaneous mitral valvulotomy (leaflet rupture of relatively thin portions of nonhomogeneously thickened leaflets in the presence of commissural and subvalvular calcification) and evaluated uneven distribution of thickness in the anterior and posterior mitral leaflets; degree of commissural disease and subvalvular disease involvement, with each component graded from 0 to 4 (total, 0 to 16). Intraobserver and interobserver variability for score assessment were 6% and 7%, respectively. Results. The total mitral regurgitation echocardiographic score was significantly greater in the severe mitral regurgitation group (11.7 +/- 1.9 [mean +/- SD] vs. 8.0 +/- 1.2, p < 0.001). In addition, the component grades for the anterior leaflet (3.2 +/- 0.7 vs. 2.3 +/- 0.6, p < 0.001), commissures (2.6 +/- 0.7 vs. 1.6 +/- 0.6, p < 0.001) and subvalvular apparatus (3.2 +/- 0.6 vs. 2.3 +/- 0.7, p < 0.001) were also higher in the mitral regurgitation group. With a total score greater than or equal to 10 as a cutoff point for predicting severe mitral regurgitation after percutaneous mitral valvulotomy, a sensitivity of 90 +/- 5% and a specificity of 97 +/- 3% were obtained. Stepwise logistic regression analysis identified the mitral regurgitation echocardiographic score as the only independent predictor for developing severe mitral regurgitation after percutaneous mitral valvulotomy (p < 0.0001). Conclusions. This new mitral regurgitation echocardiographic score can predict the development of severe mitral regurgitation after percutaneous mitral valvulotomy and can be useful in the selection of patients for this technique. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 23 TC 56 Z9 61 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1996 VL 27 IS 5 BP 1225 EP 1231 DI 10.1016/0735-1097(95)00594-3 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA UD651 UT WOS:A1996UD65100037 PM 8609347 ER PT J AU Mendez, MF AF Mendez, MF TI Dementia and guns SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID BEHAVIOR RP Mendez, MF (reprint author), UNIV CALIF LOS ANGELES,SCH MED,PSYCHIAT SERV,W LOS ANGELES VA MED CTR,DEPT NEUROL,LOS ANGELES,CA 90073, USA. NR 10 TC 13 Z9 13 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 1996 VL 44 IS 4 BP 409 EP 410 PG 2 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA UE383 UT WOS:A1996UE38300011 PM 8636586 ER PT J AU McDougal, WS AF McDougal, WS TI Influence of continent ileal urinary diversion on vitamin B12 absorption - Comment SO JOURNAL OF UROLOGY LA English DT Editorial Material RP McDougal, WS (reprint author), MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD APR PY 1996 VL 155 IS 4 BP 1208 EP 1208 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA TZ330 UT WOS:A1996TZ33000015 ER PT J AU Barry, MJ AF Barry, MJ TI Prostate disease potpourri - Measurement reliability, therapeutic effectiveness and pathophysiological diagnosis SO JOURNAL OF UROLOGY LA English DT Editorial Material ID PREDICTIVE VALUE; ANTIGEN DENSITY; ENHANCE RP Barry, MJ (reprint author), MASSACHUSETTS GEN HOSP,MED PRACTICE EVALUAT CTR,BOSTON,MA 02114, USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD APR PY 1996 VL 155 IS 4 BP 1309 EP 1310 DI 10.1016/S0022-5347(01)66253-0 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA TZ330 UT WOS:A1996TZ33000049 PM 8632562 ER PT J AU Adili, F vanEps, RGS Karp, SJ Watkins, MT LaMuraglia, GM AF Adili, F vanEps, RGS Karp, SJ Watkins, MT LaMuraglia, GM TI Differential modulation of vascular endothelial and smooth muscle cell function by photodynamic therapy of extracellular matrix: Novel insights into radical-mediated prevention of intimal hyperplasia SO JOURNAL OF VASCULAR SURGERY LA English DT Article ID FIBROBLAST GROWTH-FACTOR; PROLIFERATION; INJURY; PHTHALOCYANINE; RESTENOSIS; MIGRATION; INVITRO; ARTERY; INVIVO AB Purpose: Photodynamic therapy (PDT) has been demonstrated to inhibit experimental intimal hyperplasia and to lead to expedient reendothelialization but negligible repopulation of the vessel media. The mechanism that underlies the differential ingrowth of cells into PDT-treated vessel segments is not understood. Because the extracellular matrix (ECM) is known to modulate specific cell functions, this study was designed to determine whether PDT of isolated ECM affects the function of endothelial cells (ECs) and smooth muscle cells (SMCs). Methods: PDT of bovine aortic EC-ECM was performed with chloroaluminum sulfonated phthalocyanine and 675-nm laser light. Control specimens included untreated ECM, ECM-free plates, and ECM exposed to either light or photosensitizer only. Cell function was characterized by attachment, proliferation, and migration of ECs or SMCs that were plated onto identically treated matrixes. Results: SMC attachment (86% +/- 0.4% vs 95% +/- 0.4%), proliferation (46% +/- 0.5% vs 100% +/- 1.4%), and migration (40% +/- 1.0% vs 100% +/- 0.9%) were significantly inhibited after PDT of ECM when compared with untreated ECM (all p < 0.001). In contrast, PDT of ECM significantly enhanced EC proliferation (129% +/- 6.2% vs 100% +/- 6.2%; p < 0.03) and migration (118% +/- 1.2% vs 100% +/- 0.8; P < 0.01), but did not affect attachment. Conclusions: This report establishes PDT-induced changes in the ECM with a result of inhibition of SMCs and stimulation of EC functions. It provides insight into how PDT-treated arteries can develop favorable EC repopulation without SMC-derived intimal hyperplasia. These findings may help provide a better understanding of the interactions between cells and their immediate environment in vascular remodeling. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DIV VASC SURG, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, WELLMAN LABS PHOTOMED, BOSTON, MA 02114 USA. BOSTON UNIV, BOSTON VET ADM MED CTR, SCH MED, DIV VASC SURG, BOSTON, MA 02215 USA. FU NHLBI NIH HHS [HL 02583, HL 48152] NR 38 TC 26 Z9 27 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD APR PY 1996 VL 23 IS 4 BP 698 EP 705 DI 10.1016/S0741-5214(96)80052-8 PG 8 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA UJ126 UT WOS:A1996UJ12600024 PM 8627908 ER PT J AU Caliendo, AM Savara, A An, D DeVore, K Kaplan, JC DAquila, RT AF Caliendo, AM Savara, A An, D DeVore, K Kaplan, JC DAquila, RT TI Effects of zidovudine-selected human immunodeficiency virus type 1 reverse transcriptase amino acid substitutions on processive DNA synthesis and viral replication SO JOURNAL OF VIROLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; T-CELL ACTIVATION; ANGSTROM RESOLUTION; CRYSTAL-STRUCTURE; ESCHERICHIA-COLI; RESISTANCE; SENSITIVITY; LYMPHOCYTES; LEVEL; AZT AB Certain amino acid substitutions in the reverse transcriptase (RT), including D67N, K70R, T215Y, and K219Q, cause high-level resistance of human immunodeficiency virus type 1 (HIV-1) to zidovudine (3'-azidothymidine; AZT) and appear to approximate the template strand of the enzyme-template-primer complex is structural models. We studied whether this set of mutations altered RT-template-primer interaction as well as their effect on virus replication in the absence of inhibitor. When in vitro polymerization was limited to a single association of an RT with an oligodeoxynucleotide-primed heteropolymeric RNA template (a single processive cycle), recombinant-expressed mutant 67/70/215/219 RT synthesized 5- to 10-fold more high-molecular-weight DNA products (> 200 nucleotides in length) than wild-type RT. This advantage was maintained as deoxynucleoside triphosphate (dNTP) concentrations were decreased to limiting levels. In contrast, no difference was seen between wild-type and mutant RTs under conditions allowing repeated associations of enzyme with template-primer. Because intracellular dNTP concentrations are low prior to mitogenic stimulation, we compared replication of mutant 67/70/215/219 virus and wild-type virus in peripheral blood mono-nuclear cells (PBMC) stimulated before and after infection. In the absence of inhibitor, mutant 67/70/215/219 virus had a replication advantage in PBMC stimulated with phytohemagglutinin and interleukin-2 after infection, but virus replication was similar in PBMC stimulated before infection in vitro. The results confirm that RT mutations D67N, K70R, T215Y, and K219Q affect an enzyme-template-primer interaction in vitro and suggest that such substitutions may affect HIV-1 pathogenesis during therapy by increasing viral replication capacity in cells stimulated after infection. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. FU NIAID NIH HHS [R01 AI29193]; PHS HHS [IT 32A107387] NR 58 TC 83 Z9 84 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1996 VL 70 IS 4 BP 2146 EP 2153 PG 8 WC Virology SC Virology GA UA397 UT WOS:A1996UA39700010 PM 8642636 ER PT J AU Szurek, PF Brooks, BR AF Szurek, PF Brooks, BR TI ts1-induced spongiform encephalomyelopathy: Physical forms of high-mobility DNA in spinal cord tissues of paralyzed mice are products of premature termination of reverse transcription SO JOURNAL OF VIROLOGY LA English DT Article ID MURINE LEUKEMIA-VIRUS; SINGLE-STRANDED-DNA; TEMPERATURE SENSITIVITY; HUMAN-IMMUNODEFICIENCY; GEL-ELECTROPHORESIS; TRANSGENIC MICE; RNASE-H; T-CELL; MUTANT; TS1 AB ts1 is a temperature-sensitive mutant of Moloney murine leukemia virus that causes hind-limb paralysis in mice. In tissues of the central nervous systems of paralyzed moribund FVB/N mice, a major component of the unintegrated viral DNA of ts1 consists of highly mobile physical forms of viral-specific DNA (HM DNA). Previous studies with ecotropic virus-specific polarity probes showed that the gp70-coding region of the env gene in the HM DNA was minus-sense single-stranded DNA. The physical forms of the HM DNA have now been characterized in more detail with additional ecotropic virus-specific probes that hybridized to the p15E-coding region of the env gene and two locations within the U3 region of the long terminal repeat. Two major classes of HM DNA were found: class I molecules consist of short minus-sense single-stranded DNA; class II molecules are partial DNA duplexes that are longer than the class I molecules. The two classes of HM DNA molecules are intermediate products of reverse transcription of the viral RNA of ts1. Since tissues that are infected with cytopathic retroviruses may contain high levels of unintegrated viral DNA, the HM DNA may have a role in inducing neurodegeneration in the central nervous systems of mice that are infected with ts1. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL SERV,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,RES SERV,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT NEUROL,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT MED MICROBIOL IMMUNOL,MADISON,WI 53705. NR 49 TC 2 Z9 2 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1996 VL 70 IS 4 BP 2230 EP 2236 PG 7 WC Virology SC Virology GA UA397 UT WOS:A1996UA39700021 PM 8642647 ER PT J AU Grellier, P Sabbah, M Fouqueray, B Woodruff, K Yee, D Abboud, HE Abboud, SL AF Grellier, P Sabbah, M Fouqueray, B Woodruff, K Yee, D Abboud, HE Abboud, SL TI Characterization of insulin-like growth factor binding proteins and regulation of IGFBP3 in human mesangial cells SO KIDNEY INTERNATIONAL LA English DT Article ID MESSENGER-RIBONUCLEIC-ACID; OSTEOBLAST-LIKE CELLS; BREAST-CANCER CELLS; FACTOR-I; HUMAN FIBROBLASTS; RNA EXPRESSION; STROMAL CELLS; DNA-SYNTHESIS; FACTOR-BETA; KIDNEY AB IGF-I regulates renal growth and development. Insulin-like growth factor binding proteins (IGFBPs) are synthesized by the kidney and may modulate the local autocrine and/or paracrine actions of IGF-I. We have previously demonstrated that mesangial cells (MC) release IGF-I and IGF-binding activity; however, the specific IGFBPs produced by these cells and the factors involved in their regulation are unknown. We examined MC for expression of IGFBP-1 to -6 mRNAs and proteins. RNase protection assays using total RNA demonstrated that MC express all of the IGFBPs. [I-125]IGF-I Western ligand blot of conditioned medium demonstrated that MC release IGFBPs of 24, 29, 32 kDa, and a doublet at 46 kDa, consistent with IGFBP-4 -5, -2 and -3, respectively. IGFBP species of 28 and 34 kDa were also detected. Since IGF-I and TGF-beta are implicated in glomerular hypertrophy and matrix expansion, we tested their effect on IGFBPs released by MC. IGF-I (100 ng/ml), TGF-beta (2 ng/ml) and forskolin (10(-5) M) differentially regulated the abundance of IGFBPs released in the conditioned medium in a time-dependent manner. IGF-I and TGF-beta were potent inducers of the release of IGFBP3 protein; however, TGF-beta, but not IGF-I, increased IGFBP3 mRNA levels. Recombinant IGFBP3 was tested for its effect on IGF-I-induced mitogenesis. IGFBP3 inhibited IGF-I-stimulated DNA synthesis in a dose-dependent manner with a peak effect observed at 50 nM IGFBP3. Although TGF-beta is a potent inhibitor of IGF-I-stimulated DNA synthesis, this effect is not mediated via IGFBPs. Expression of IGFBP-1 to -6 by MC suggests that these proteins may modulate IGF-I bioavailability in the glomerulus. IGF-I itself, TGF-beta and cAMP agonists may indirectly modulate the effects of IGF-I via the release of IGFBPs by MC. C1 UNIV TEXAS, HLTH SCI CTR, DEPT MED, SAN ANTONIO, TX 78284 USA. UNIV TEXAS, HLTH SCI CTR, DEPT PATHOL, SAN ANTONIO, TX 78284 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. FU NCI NIH HHS [CA52952]; NIAMS NIH HHS [AR42306]; NIDDK NIH HHS [DK33665] NR 44 TC 19 Z9 19 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 0085-2538 EI 1523-1755 J9 KIDNEY INT JI Kidney Int. PD APR PY 1996 VL 49 IS 4 BP 1071 EP 1078 DI 10.1038/ki.1996.156 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA UB112 UT WOS:A1996UB11200027 PM 8691727 ER PT J AU Li, KK Schwartz, HC AF Li, KK Schwartz, HC TI Mandibular body bone in facial plastic and reconstructive surgery SO LARYNGOSCOPE LA English DT Article ID ENDOCHONDRAL BONE; DONOR-SITE; MORBIDITY; GRAFTS; RIB C1 SO CALIF PERMANENTE MED GRP,DEPT MAXILLOFACIAL SURG,LOS ANGELES,CA 90027. RP Li, KK (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTORHINOLARYNGOL HEAD & NECK SURG,BOSTON,MA 02115, USA. NR 14 TC 9 Z9 9 U1 0 U2 1 PU LARYNGOSCOPE CO PI ST LOUIS PA 10 S BROADWAY 14TH FLOOR, ST LOUIS, MO 63102-1741 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD APR PY 1996 VL 106 IS 4 BP 504 EP 506 DI 10.1097/00005537-199604000-00022 PG 3 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA UM980 UT WOS:A1996UM98000037 PM 8614231 ER PT J AU Ubel, PA Loewenstein, G Scanlon, D Kamlet, M AF Ubel, PA Loewenstein, G Scanlon, D Kamlet, M TI Individual utilities are inconsistent with rationing choices: A partial explanation of why Oregon's cost-effectiveness list failed SO MEDICAL DECISION MAKING LA English DT Article ID HEALTH STATES; PREFERENCES; ELICITATION; THERAPIES AB Objective. To test whether cost-effectiveness analysis and present methods of eliciting health condition ''utilities'' capture the public's values for health care rationing. Design. Two surveys of economics students. The first survey measured their utilities for three states of health, using either analog scale, standard gamble, or time tradeoff. The second survey measured their preferences, in paired rationing choices of the health states from the first survey and also compared with treatment of acutely fatal appendicitis. The rationing choices each subject faced were individualized according to his or her utility responses, so that the subject should have been indifferent between the two conditions in each rationing choice. Results. The analog-scale elicitation method produced significantly lower utilities than the time-tradeoff and standard-gamble methods for two of the three conditions (p < 0.001). Compared with the rationing choices, all three utility-elicitation methods placed less value on the importance of saving lives and treating more severely ill people compared with less severely ill ones (p < 0.0001). The subjects' rationing choices indicated that they placed values on treating severely ill people that were tenfold to one-hundred-thousand-fold greater than would have been predicted by their utility responses. However, the subjects' rationing choices showed internal inconsistency, as, for example, treatments that were indicated to be ten times more beneficial in one scenario were valued as one hundred times more beneficial in other scenarios. Conclusions. The subjects soundly rejected the rationing choices derived from their utility responses. This suggests that people's answers to utility elicitations cannot be easily translated into social policy. However, person-tradeoff elicitations, like those given in our rationing survey, cannot be substituted for established methods of utility elicitation until they can be performed in ways that yield acceptable internal consistency. C1 VET AFFAIRS MED CTR, PHILADELPHIA, PA USA. UNIV PENN, CTR BIOETH, CTR CLIN EPIDEMIOL & BIOSTAT, DIV GEN INTERNAL MED, PHILADELPHIA, PA 19104 USA. UNIV PENN, LEONARD DAVIS INST HLTH ECON, PHILADELPHIA, PA 19104 USA. CARNEGIE MELLON UNIV, DEPT SOCIAL & DECIS SCI, PITTSBURGH, PA 15213 USA. UNIV MICHIGAN, SCH PUBL HLTH, ANN ARBOR, MI 48109 USA. CARNEGIE MELLON UNIV, H JOHN HEINZ III SCH PUBL POLICY & MANAGEMENT, PITTSBURGH, PA 15213 USA. NR 27 TC 79 Z9 79 U1 0 U2 3 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0272-989X J9 MED DECIS MAKING JI Med. Decis. Mak. PD APR-JUN PY 1996 VL 16 IS 2 BP 108 EP 116 DI 10.1177/0272989X9601600202 PG 9 WC Health Care Sciences & Services; Medical Informatics SC Health Care Sciences & Services; Medical Informatics GA UC889 UT WOS:A1996UC88900002 PM 8778528 ER PT J AU Hiebert, SW Sun, WH Davis, JN Golub, T Shurtleff, S Buijs, A Downing, JR Grosveld, G Roussel, MF Gilliland, DG Lenny, N Meyers, S AF Hiebert, SW Sun, WH Davis, JN Golub, T Shurtleff, S Buijs, A Downing, JR Grosveld, G Roussel, MF Gilliland, DG Lenny, N Meyers, S TI The t(12;21) translocation converts AML-1B from an activator to a repressor of transcription SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ACUTE MYELOID-LEUKEMIA; DNA-BINDING; AML1 GENE; DROSOPHILA; IDENTIFICATION; PROTEIN; FUSION; CELLS; RUNT; BREAKPOINTS AB The t(12;21) translocation is present in up to 30% of childhood B-cell acute lymphoblastic leukemias and fuses a potential dimerization motif from the ets-related factor TEL to the N terminus of AML1. The t(12;21) translocation encodes a 93-kDa fusion protein that localizes to a high-salt- and detergent-resistant nuclear compartment. This protein binds the enhancer core motif, TGTGGT, and interacts with the AML-l-binding protein, core-binding factor beta. Although TEL/AML-1B retains the C-terminal domain of AML-1B that is required for transactivation of the T-cell receptor beta enhancer, it fails to activate transcription but rather inhibits the basal activity of this enhancer. TEL/AML-1B efficiently interferes with AML-1B-dependent transactivation of the T-cell receptor beta enhancer, and coexpression of wild-type TEL does not reverse this inhibition. The N-terminal TEL helix-loop-helix domain is essential for TEL/AML-1B-mediated repression. Thus, the t(12;21) fusion protein dominantly interferes with AML-1B-dependent transcription, suggesting that the inhibition of expression of AML-1 target genes is critical for B-cell leukemogenesis. C1 ST JUDE CHILDRENS RES HOSP, DEPT PATHOL, MEMPHIS, TN 38105 USA. ST JUDE CHILDRENS RES HOSP, DEPT GENET, MEMPHIS, TN 38105 USA. HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DIV HEMATOL ONCOL, BOSTON, MA 02115 USA. HARVARD UNIV, CHILDRENS HOSP, SCH MED, DIV PEDIAT HEMATOL ONCOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. RP Hiebert, SW (reprint author), ST JUDE CHILDRENS RES HOSP, DEPT TUMOR CELL BIOL, MEMPHIS, TN 38105 USA. RI Hiebert, Scott/C-9979-2010 FU NCI NIH HHS [CA-57261, R01 CA-56819, R01 CA-64140] NR 55 TC 221 Z9 221 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1996 VL 16 IS 4 BP 1349 EP 1355 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UB562 UT WOS:A1996UB56200008 PM 8657108 ER PT J AU Blobel, GA Orkin, SH AF Blobel, GA Orkin, SH TI Estrogen-induced apoptosis by inhibition of the erythroid transcription factor GATA-1 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID CELLULAR P53 GENE; GLUCOCORTICOID RECEPTOR; ERYTHROPOIETIN RECEPTOR; DNA FRAGMENTATION; FRIEND-VIRUS; STEM-CELLS; C-JUN; EXPRESSION; DEATH; BCL-2 AB Steroid hormones regulate diverse biological functions, including programmed cell death (apoptosis). Although steroid receptors have been studied extensively, relatively little is known regarding the cellular targets through which apoptosis is triggered, We show here that the ligand-activated estrogen receptor (ER) induces apoptosis in an erythroid cell line by binding to, and consequently inhibiting the activity of, GATA-1, an erythroid transcription factor essential for the survival and maturation of erythroid precursor cells, GATA-1 inhibition is reflected in the downregulation of presumptive GATA-1 target genes, Constitutive overexpression of a GATA-binding protein resistant to the effects of the ER partially rescues ER-induced apoptosis, Induction of apoptosis by a mutant ER defective in binding to the estrogen response element but active in GATA-1 inhibition suggests that ER-mediated inhibition of GATA-1 is direct and does not require estrogen response element-dependent transcriptional activation, Thus, a lineage-restricted transcription factor, such as GATA-1, constitutes one cellular target through which steroid hormones may control apoptosis, As GATA-binding proteins are evolutionarily conserved, we speculate that members of the steroid receptor family may exert some of their diverse biological functions in different cellular contexts through interference with the function of GATA-binding proteins. C1 CHILDRENS HOSP,DANA FARBER CANC INST,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA 02115. NR 60 TC 82 Z9 83 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1996 VL 16 IS 4 BP 1687 EP 1694 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UB562 UT WOS:A1996UB56200044 PM 8657144 ER PT J AU Crossley, M Whitelaw, E Perkins, A Williams, G Fujiwara, Y Orkin, SH AF Crossley, M Whitelaw, E Perkins, A Williams, G Fujiwara, Y Orkin, SH TI Isolation and characterization of the cDNA encoding BKLF/TEF-2, a major CACCC-box-binding protein in erythroid cells and selected other cells SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PORPHOBILINOGEN DEAMINASE GENE; TRANSCRIPTION FACTOR; GLUCOCORTICOID RECEPTOR; NUCLEAR PROTEINS; DNA INTERACTIONS; INVIVO PROTEIN; CONTROL REGION; GLOBIN GENE; PROMOTER; ELEMENT AB CACCC boxes are among the critical sequences present in regulatory elements of genes expressed in erythroid cells, as well as in selected other cell types. While an erythroid cell-specific CACCC-box-binding protein, EKLF, has been shown to be required in vivo for proper expression of the adult beta-globin gene, it is dispensable for the regulation of several other globin and nonglobin erythroid cell-expressed genes. In the work described here, we searched for additional CACCC-box transcription factors that might be active in murine erythroid cells. We identified a major gel shift activity (termed BKLF), present in yolk sac and fetal liver erythroid cells, that could be distinguished from EKLF by specific antisera. Through relaxed-stringency hybridization, we obtained the cDNA encoding BKLF, a highly basic, novel zinc finger protein that is related to EKLF and other Kruppel-like members in its DNA-binding domain but unrelated elsewhere. BKLF, which is widely but not ubiquitously expressed in cell lines, is highly expressed in the midbrain region of embryonic mice and appears to correspond to the gel shift activity TEF-2, a transcriptional activator implicated in regulation of the simian virus 40 enhancer and other CACCC-box-containing regulatory elements. Because BKLF binds with high affinity and preferentially over Sp1 to many CACCC sequences of erythroid cell-expressed genes, it is likely to participate in the control of many genes whose expression appears independent of the action of EKLF. C1 CHILDRENS HOSP,DANA FARBER CANC INST,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT PEDIAT,BOSTON,MA 02115. UNIV SYDNEY,DEPT BIOCHEM,SYDNEY,NSW 2006,AUSTRALIA. RI Crossley, Merlin/D-7888-2011; Perkins, Andrew/M-3216-2014 OI Crossley, Merlin/0000-0003-2057-3642; Perkins, Andrew/0000-0003-3644-7093 NR 40 TC 185 Z9 190 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1996 VL 16 IS 4 BP 1695 EP 1705 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UB562 UT WOS:A1996UB56200045 PM 8657145 ER PT J AU BenEliyahu, S Page, GG Yirmiya, R Taylor, AN AF BenEliyahu, S Page, GG Yirmiya, R Taylor, AN TI Acute alcohol intoxication suppresses natural killer cell activity and promotes tumor metastasis SO NATURE MEDICINE LA English DT Article ID MONOCLONAL-ANTIBODY; NK CELLS; RATS; CANCER; INVIVO; ETHANOL; INVOLVEMENT; IMMUNITY; DEFENSE; SPREAD AB Alcohol consumption is associated with increased morbidity and mortality related to infectious diseases and malignancy(1-5), although immune mediation of these relationships is controversial. Specifically, the activity of natural killer (NK) cells, which are involved in the resistance to infections and metastasis, can be suppressed in the presence of ethanol in vitro. However, acute consumption or infusion of ethanol in vivo exerts no effects on NK activity assessed in vitro thereafter. Therefore, we have developed and used a method to study the effects of ethanol on NK activity in living rats by using an NK-sensitive metastatic process and selective depletion of NK cells in vivo. Acute ethanol intoxication caused a-marked suppression of NK activity in vivo and a tenfold increase in the number of MADB106 tumor metastases. Ethanol had no effect in rats selectively depleted of NK cells or when an NK-insensitive tumor (C4047) was used. These findings suggest that even acute ethanol intoxication markedly suppresses NK activity in the living organism. This suppression may underlie some aspects of the association between alcoholism, infectious disease and malignancies. C1 OHIO STATE UNIV,COLL NURSING,COLUMBUS,OH 43210. HEBREW UNIV JERUSALEM,DEPT PSYCHOL,IL-91905 JERUSALEM,ISRAEL. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROBIOL,LOS ANGELES,CA 90095. W LOS ANGLES DEPT VET AFFAIRS MED CTR,LOS ANGELES,CA 90095. RP BenEliyahu, S (reprint author), TEL AVIV UNIV,DEPT PSYCHOL,IL-69978 TEL AVIV,ISRAEL. RI Yirmiya, Raz/D-1090-2014 FU NCI NIH HHS [CA 16042] NR 35 TC 88 Z9 90 U1 0 U2 2 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD APR PY 1996 VL 2 IS 4 BP 457 EP 460 DI 10.1038/nm0496-457 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA UD314 UT WOS:A1996UD31400049 PM 8597957 ER PT J AU Breton, S Smith, PJS Lui, B Brown, D AF Breton, S Smith, PJS Lui, B Brown, D TI Acidification of the male reproductive tract by a proton pumping (H+)-ATPase SO NATURE MEDICINE LA English DT Article ID ANHYDRASE-II DEFICIENCY; CARBONIC-ANHYDRASE; HISTOCHEMICAL-LOCALIZATION; SPERM MOTILITY; RAT EPIDIDYMIS; H+-ATPASE; PH; TESTIS; KIDNEY; CELLS AB An acidic luminal pH (ref. 1-3) is involved in sperm maturation, and in maintaining sperm in an immotile state in the epididymis and vas deferens(2,4-6). Neutralization by prostatic fluid is one of a complex series of events that triggers sperm motility(2,7,8). Failure of the acidification mechanism might, therefore, result in poor sperm maturation, premature motility and infertility. We have shown that a vacuolar (H+)-ATPase is expressed at high levels on the luminal plasma membrane of specialized cells in the epididymis(9), which closely resemble acid-secreting kidney intercalated cells(10.11). We now show that similar cells are also present in the vas deferens, and that a bafilomycin-sensitive proton flux can be detected using a noninvasive proton-selective vibrating probe. Up to 80% of the net proton secretion in the vas deferens is inhibited by bafilomycin, consistent with a major role of a vacuolar-type (H+)-ATPase in this process. This acidification mechanism is a potential target for novel strategies aimed at modulating the acidification capacity of parts of the male reproductive tract and, therefore, in regulating male fertility. C1 HARVARD UNIV, SCH MED, BOSTON, MA 02129 USA. MASSACHUSETTS GEN HOSP, RENAL UNIT, BOSTON, MA 02129 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02129 USA. MARINE BIOL LAB, NATL VIBRATING PROBE FACIL, WOODS HOLE, MA 02543 USA. FU NIDDK NIH HHS [DK 42956] NR 23 TC 188 Z9 191 U1 1 U2 7 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 1078-8956 EI 1546-170X J9 NAT MED JI Nat. Med. PD APR PY 1996 VL 2 IS 4 BP 470 EP 472 DI 10.1038/nm0496-470 PG 3 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA UD314 UT WOS:A1996UD31400053 PM 8597961 ER PT J AU Zhou, MM Huang, BH Olejniczak, ET Meadows, RP Shuker, SB Miyazaki, M Trub, T Shoelson, SE Fesik, SW AF Zhou, MM Huang, BH Olejniczak, ET Meadows, RP Shuker, SB Miyazaki, M Trub, T Shoelson, SE Fesik, SW TI Structural basis for IL-4 receptor phosphopeptide recognition by the IRS-1 PTB domain SO NATURE STRUCTURAL BIOLOGY LA English DT Article ID DISTANCE GEOMETRY AB We present the NMR structure of the PTB domain of insulin receptor substrate-1 (IRS-1) complexed to a tyrosine-phosphorylated peptide derived from the IL-4 receptor. Despite the lack of sequence homology and different binding specificity, the overall fold of the protein is similar to that of the Shc PTB domain and closely resembles that of PH domains. However, the PTB domain of IRS-1 is smaller than that of Shc (110 Versus 170 residues) and binds to phosphopeptides in a distinct manner. We explain the phosphopeptide binding specificity based on the structure of the complex and results of site-directed mutagenesis experiments. C1 ABBOTT LABS,DIV PHARMACEUT DISCOVERY,ABBOTT PK,IL 60064. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02215. RI Miyazaki, Masaya/F-8520-2012 OI Miyazaki, Masaya/0000-0003-4031-7224 NR 33 TC 117 Z9 121 U1 0 U2 2 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1072-8368 J9 NAT STRUCT BIOL JI Nat. Struct. Biol. PD APR PY 1996 VL 3 IS 4 BP 388 EP 393 DI 10.1038/nsb0496-388 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA UD310 UT WOS:A1996UD31000018 PM 8599766 ER PT J AU Liu, ZH Striker, LJ Hattori, M Yang, CW Striker, GE AF Liu, ZH Striker, LJ Hattori, M Yang, CW Striker, GE TI Localization of glutamic acid decarboxylase in the kidneys of nonobese diabetic mice SO NEPHRON LA English DT Article DE glutamic acid decarboxylase; nonobese diabetic mice; insulin-dependent diabetes mellitus; kidney; polymerase chain reaction; tubulointerstitial disease; glomerulus ID PANCREATIC BETA-CELLS; SYNAPTIC-LIKE MICROVESICLES; MOUSE; IDENTIFICATION; AUTOIMMUNITY; EXPRESSION; MELLITUS; TISSUES; ENZYME; FORMS AB Antibodies to glutamic acid decarboxylase (GAD), a pancreatic islet beta-cell antigen, are present in >80% of newly diagnosed insulin-dependent diabetes mellitus (IDDM), and are found in nonobese diabetic (NOD) mice, a murine model of spontaneous IDDM. To determine whether GAD is a target antigen in the kidney damage of NOD mice, we studied GAD mRNAs (GAD(65) and GAD(67)) by RT-PCR in mesangial cells, isolated glomeruli, and kidney cortex and medulla in NOD and SJL/C57BL mice. GAD mRNAs were detected in the cortex of both diabetic and nondiabetic NOD and SJL/C57BL mice and GAD antigen was present in proximal and distal tubules by immunofluorescence microscopy. Neither GAD antigen nor mRNA were present in mesangial cells or glomeruli of diabetic or nondiabetic mice. Thus, the expression of GAD in renal tubules raises the possibility that GAD antigens may play a role in diabetic tubulointerstitial disease, whereas the absence of these antigens in glomeruli suggests that CAD-triggered autoimmunity is not directly involved in the glomerular lesions. C1 NIDDKD,NIH,METAB DIS BRANCH,RENAL CELL BIOL SECT,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,SECT IMMUNOL & IMMUNOGENET,BOSTON,MA 02115. FU NIDDK NIH HHS [R01DK36836, R01DK43613] NR 31 TC 8 Z9 9 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-2766 J9 NEPHRON JI Nephron PD APR PY 1996 VL 72 IS 4 BP 662 EP 666 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA UD213 UT WOS:A1996UD21300028 PM 8730438 ER PT J AU Lo, EH Rogowska, J Batchelder, KF Wolf, GL AF Lo, EH Rogowska, J Batchelder, KF Wolf, GL TI Hemodynamic alterations in focal cerebral ischemia: Temporal correlation analysis for functional imaging SO NEUROLOGICAL RESEARCH LA English DT Article DE cerebral blood flow; functional CT; ischemic penumbra; stroke ID COMPUTED-TOMOGRAPHY; ARTERY OCCLUSION; BRAIN; RATS; THRESHOLDS; INFARCTION; INJURY AB We describe a novel approach for analysing the hemodynamic alterations that result after focal cerebral ischemia. This approach utilizes a temporal correlation analysis of first pass transit data obtained with functional imaging. First pass transits of injected contrast agents are measured with dynamic CT scanning. Normal transit profiles are obtained from contralateral cortical regions to serve as reference profiles. Normalized correlations are then calculated to compare transit profiles from each individual pixel within the brain to the normal reference profile. The normalized correlation coefficient is used as a measure of temporal similarity to quantitatively assess deviations from normal hemodynamics. The method is based on the premise that perturbed hemodynamics are manifested as changes in the shape of the cerebral transit profiles. Correlation maps are produced that display regional alterations in cerebral hemodynamics. Results from rabbit (n = 4) and rat (n = 4) models of focal ischemia are presented. In the normal contralateral hemisphere, correlation values range from 0.83-0.93 with coefficients of variation of less than 3-4%. The ischemic core is comprised of regions without significant bolus transit The peripheral zones that lie between normal brain and the ischemic core are composed of intermediate correlation values. By setting statistical thresholds (mean minus 2SD, p < 0.05), we quantitatively define these intermediate zones as the hemodynamic penumbra, i.e. regions where the shape of the first pass transit profile has been altered. The resulting correlation maps clearly image gradients of altered cerebral hemodynamics. Perfusion indices calculated based on transit profile peaks revealed that the penumbral zones possess reduced perfusion on the order of about 40% of contralateral values. In summary, we believe that temporal correlation analysis of first pass transit profiles can be used to image the hemodynamic penumbra in focal cerebral ischemia. RP Lo, EH (reprint author), HARVARD UNIV,SCH MED,CTR IMAGING & PHARMACEUT RES,MASSACHUSETTS GEN HOSP,DEPT RADIOL,MGH E 149,BOSTON,MA 02129, USA. NR 37 TC 10 Z9 12 U1 0 U2 0 PU FOREFRONT PUBL GROUP PI LONDON PA MONOMARK HOUSE 27 OLD GLOUCESTER STREET, LONDON, ENGLAND WC1N 3XX SN 0161-6412 J9 NEUROL RES JI Neurol. Res. PD APR PY 1996 VL 18 IS 2 BP 150 EP 156 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA UF152 UT WOS:A1996UF15200009 PM 9162870 ER PT J AU Litvan, I Agid, Y Jankovic, J Goetz, C Brandel, JP Lai, EC Wenning, G DOlhaberriague, L Verny, M Chaudhuri, KR McKee, A Jellinger, K Bartko, JJ Mangone, CA Pearce, RKB AF Litvan, I Agid, Y Jankovic, J Goetz, C Brandel, JP Lai, EC Wenning, G DOlhaberriague, L Verny, M Chaudhuri, KR McKee, A Jellinger, K Bartko, JJ Mangone, CA Pearce, RKB TI Accuracy of clinical criteria for the diagnosis of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) SO NEUROLOGY LA English DT Article ID LEWY BODY DISEASE; ALZHEIMERS-DISEASE; GAZE PALSY; DEMENTIA; PARKINSONISM; DEGENERATION; TANGLES AB We assessed the validity and interrater reliability of neurologists who, using four different sets of previously published criteria for the clinical diagnosis of progressive supranuclear palsy (PSP), also called Steele-Richardson-Olszewski syndrome, rated 105 autopsy-proven cases of PSP (n = 24), Lewy body disease (n = 29), corticobasal ganglionic degeneration (n = 10), postencephalitic parkinsonism (n = 7), multiple system atrophy (n = 16), Pick's disease (n = 7), and other parkinsonian or dementia disorders (n = 12). Cases were presented in random order to six neurologists. Information from each patient's first and last visits to the medical center supplying the case was presented sequentially to the rater, and the rater's diagnosis was compared with the neuropathologic diagnosis of each case. Interrater agreement for the diagnosis of PSP varied from substantial to near perfect, but none of the criteria had both high sensitivity and high predictive value. Because of these limitations, we used a logistic regression analysis to identify the variables from the data set that would best predict the diagnosis. This analysis identified vertical supranuclear palsy with downward gaze abnormalities and postural instability with unexplained falls as the best features for predicting the diagnosis. From the results of the regression analysis and the addition of exclusionary features, we propose optimal criteria for the clinical diagnosis of PSP. C1 HOP LA PITIE SALPETRIERE,INSERM,U289,F-75651 PARIS,FRANCE. HOP LA PITIE SALPETRIERE,FEDERAT NEUROL,PARIS,FRANCE. BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030. RUSH MED COLL,DEPT NEUROL,CHICAGO,IL 60612. INST NEUROL,PARKINSONS DIS SOC BRAIN TISSUE BANK,LONDON WC1N 3BG,ENGLAND. INST PSYCHIAT,DEPT NEUROL,LONDON SE5 8AF,ENGLAND. HOP LA PITIE SALPETRIERE,RAYMOND ESCOUROLLE NEUROPATHOL LAB,INSERM U360,PARIS,FRANCE. MASSACHUSETTS GEN HOSP,DEPT NEUROPATHOL,BOSTON,MA 02114. LUDWIG BOLTZMANN INST CLIN NEUROBIOL,VIENNA,AUSTRIA. NIMH,DIV EPIDEMIOL & SERV RES,BETHESDA,MD 20892. RP Litvan, I (reprint author), NINCDS,NEUROEPIDEMIOL BRANCH,NIH,FED BLDG,ROOM 714,BETHESDA,MD 20814, USA. OI Litvan, Irene/0000-0002-3485-3445; Ray Chaudhuri, K/0000-0003-2815-0505 NR 58 TC 237 Z9 240 U1 0 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1996 VL 46 IS 4 BP 922 EP 930 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA UG635 UT WOS:A1996UG63500007 PM 8780065 ER PT J AU Morens, DM Davis, JW Grandinetti, A Ross, GW Popper, JS White, LR AF Morens, DM Davis, JW Grandinetti, A Ross, GW Popper, JS White, LR TI Epidemiologic observations on Parkinson's disease: Incidence and mortality in a prospective study of middle-aged men SO NEUROLOGY LA English DT Article ID PREVALENCE; CITY AB We determined age-specific and age-adjusted incidence rates and mortality rates of idiopathic Parkinson's disease (PD)in a cohort of men followed for 29 years. Since enrollment in 1965, the Honolulu Heart Study has followed 8,006 American men of Japanese or Okinawan ancestry. Rescreening of the entire cohort, completed in 1994, included attempts to detect all prevalent and incident cases of PD, parkinsonism, and related conditions. PD incidence rates and age-incidence patterns were similar to rates previously published for Caucasian men in Europe and the United States, and were higher than incidence rates published for Asian men living in Asian nations; Prevalence patterns appeared to correspond more closely to patterns observed in developed nations than in Asian nations. PD was associated with markedly increased mortality that appeared to result from effects of both absolute age and disease duration. There was no firm evidence for differences in birth cohort risks of PD. These data may have implications for maturational and environmental theories of PD etiology. C1 UNIV HAWAII,SCH MED,HONOLULU,HI 96822. HAWAII OSTEOPOROSIS CTR,HONOLULU,HI. EAST WEST CTR,HONOLULU,HI 96822. UNIV HAWAII,PACIFIC BIOMED RES CTR,HONOLULU,HI 96822. HONOLULU ASIA AGING STUDY,HONOLULU,HI 96822. US DEPT VET AFFAIRS,HONOLULU,HI 96822. NIA,NIH,HONOLULU,HI 96822. RP Morens, DM (reprint author), UNIV HAWAII,SCH PUBL HLTH,PROGRAM EPIDEMIOL,BIOMED D103,1960 EAST WEST RD,HONOLULU,HI 96822, USA. FU NINDS NIH HHS [NS-30371] NR 26 TC 105 Z9 111 U1 0 U2 6 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1996 VL 46 IS 4 BP 1044 EP 1050 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA UG635 UT WOS:A1996UG63500030 PM 8780088 ER PT J AU MacCollin, M Woodfin, W Kronn, D Short, MP AF MacCollin, M Woodfin, W Kronn, D Short, MP TI Schwannomatosis: A clinical and pathologic study SO NEUROLOGY LA English DT Article ID BILATERAL ACOUSTIC NEUROFIBROMATOSIS; MULTIPLE CUTANEOUS NEURILEMMOMAS; VONRECKLINGHAUSENS DISEASE; GENE; TYPE-2 AB Schwannomas are benign nerve sheath tumors that most commonly occur singularly in otherwise normal individuals. Multiple schwannomas in a single patient are most often seen in neurofibromatosis 2 (NF2), but several recent reports suggest that schwannomatosis may also be a distinct clinical entity. We studied the clinical, radiographic, and pathologic features of 14 patients with multiple schwannomas who did not have vestibular schwannoma diagnostic of NF2. Most patients had peripheral nerve tumors that presented with pain. Many also had spinal nerve root and cranial nerve tumors. Three had multiple tumors limited to a single limb, We found that these 14 individuals did not exhibit phenotypic overlap with the neurofibromatoses. Only 1 of 14 patients had a positive family history. We conclude that patients with multiple schwannomas, who do not have vestibular schwannoma, comprise a distinct clinical problem, but further molecular genetic analysis is needed to define the pathophysiology of this disorder. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NEUROL CLIN TEXAS,DEPT NEUROL,DALLAS,TX. NYU,MED CTR,DIV HUMAN GENET,NEW YORK,NY 10016. NR 41 TC 126 Z9 132 U1 0 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1996 VL 46 IS 4 BP 1072 EP 1079 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA UG635 UT WOS:A1996UG63500036 PM 8780094 ER PT J AU Segal, AZ Rordorf, G AF Segal, AZ Rordorf, G TI Gabapentin as a novel treatment for postherpetic neuralgia SO NEUROLOGY LA English DT Article RP Segal, AZ (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,WACC 835,BOSTON,MA 02114, USA. NR 7 TC 84 Z9 88 U1 0 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1996 VL 46 IS 4 BP 1175 EP 1176 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA UG635 UT WOS:A1996UG63500063 PM 8780121 ER PT J AU Liu, Y Jurman, ME Yellen, G AF Liu, Y Jurman, ME Yellen, G TI Dynamic rearrangement of the outer mouth of a K+ channel during gating SO NEURON LA English DT Article ID POTASSIUM CHANNEL; CYSTEINE-SUBSTITUTION; SENSORY RECEPTOR; BINDING-SITE; TEA BLOCKADE; INACTIVATION; BLOCKING; MUTANTS; REGION; MECHANISMS AB With prolonged stimulation, voltage-activated Ki channels close by a gating process called inactivation. This inactivation gating can occur by two distinct molecular mechanisms: N-type, in which a tethered particle blocks the intracellular mouth of the pore, and C-type, which involves a closure of the external mouth. The functional motion involved in C-type inactivation was studied by introducing cysteine residues at the outer mouth of Shaker K+ channels through mutagenesis, and by measuring state-dependent changes in accessibility to chemical modification. Modification of three adjacent residues in the outer mouth was 130-10,000-fold faster in the C-type inactivated state than in the closed state. At one position, state-dependent bridging or disulfide crosslinking between subunits was also possible. These results give a consistent picture in which C-type inactivation promotes a local rearrangement and constriction of the channel at the outer mouth. RP HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT NEUROBIOL, BOSTON, MA 02114 USA. OI Yellen, Gary/0000-0003-4228-7866 FU NINDS NIH HHS [NS09774, NS29693, R01 NS029693] NR 40 TC 369 Z9 373 U1 1 U2 6 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0896-6273 EI 1097-4199 J9 NEURON JI Neuron PD APR PY 1996 VL 16 IS 4 BP 859 EP 867 DI 10.1016/S0896-6273(00)80106-3 PG 9 WC Neurosciences SC Neurosciences & Neurology GA UG611 UT WOS:A1996UG61100019 PM 8608004 ER PT J AU Tsuchiya, T Kishimoto, J Granstein, RD Nakayama, Y AF Tsuchiya, T Kishimoto, J Granstein, RD Nakayama, Y TI Quantitative analysis of cutaneous calcitonin gene-related peptide content in response to acute cutaneous mechanical or thermal stimuli and immobilization-induced stress in rats SO NEUROPEPTIDES LA English DT Article ID PRIMARY SENSORY NEURONS; IMMUNOREACTIVE NERVE-FIBERS; SUBSTANCE-P; MAST-CELLS; ANESTHETIZED RATS; SKIN; CAPSAICIN; PSORIASIS; RELEASE; TISSUE AB The effects of various stimuli on restricted skin areas or immobilization-induced stress on the calcitonin gene-related peptide (CGRP) content in rat skin were examined by radioimmunoassay (RIA) and immunohistochemistry. Various stimuli were delivered to the shaven skin of the medial thigh by pinching, brushing, or contact with a glass tube containing hot (50 degrees C) or ice-water for 2 min. To induce immobilization stress, animals were placed in the prone position and wrapped with flexible wire gauze at room temperature. The cutaneous CGRP content determined by RIA as well as the number of CGRP-immunoreactive nerve fibers of the skin were significantly higher at sites stimulated by pinching or ice-water compared to non-stimulated areas within the same animals. However, after brushing, hot water stimulation or any period (2 min, 30 min, 2 h, 6 h, or 3 days x 6 h) of immobilization stress, no differences in cutaneous CGRP content were observed. Plasma corticosterone levels increased after immobilization stress of 30 min or greater, but plasma CGRP level did not change after any period of immobilization stress. These data suggest that some forms of cutaneous stimulation cause a rapid rise in CGRP content in the skin, while emotional stress does not influence the cutaneous CGRP content. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,CAMBRIDGE,MA 02138. RP Tsuchiya, T (reprint author), SHISEIDO RES CTR,LIFE SCI RES LABS,KANAZAWA KU,1-12-1 FUKURA,YOKOHAMA,KANAGAWA 236,JAPAN. FU NIAMS NIH HHS [AR 42429] NR 46 TC 9 Z9 10 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0143-4179 J9 NEUROPEPTIDES JI Neuropeptides PD APR PY 1996 VL 30 IS 2 BP 149 EP 157 DI 10.1016/S0143-4179(96)90082-7 PG 9 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA UN984 UT WOS:A1996UN98400006 PM 8771557 ER PT J AU Reeves, SA Ueki, K Sinha, B Difiglia, M Louis, DN AF Reeves, SA Ueki, K Sinha, B Difiglia, M Louis, DN TI Regional expression and subcellular localization of the tyrosine-specific phosphatase SH-PTP2 in the adult human nervous system SO NEUROSCIENCE LA English DT Article DE brain; SH-PTP2; PTP1D; human; expression; neurons ID CILIARY NEUROTROPHIC FACTOR; PHOSPHOTYROSINE PHOSPHATASE; SEQUENCE SIMILARITY; SH2 DOMAIN; PROTEIN; SURVIVAL; CYTOKINES; CORKSCREW; SYP AB The protein tyrosine phosphatase SH-PTP2 has been implicated in a variety of cell signaling cascades, including those mediating neuronal survival. We therefore investigated the expression of SH-PTP2 in the adult human nervous system using Western blotting, immunohistochemistry and immunoelectron microscopy. SH-PTP2 immunoreactivity was noted only in neurons, but was not restricted to a specific neuronal type or location. Immunohistochemistry showed perikaryal staining, whereas Western blotting and ultrastructural analysis suggested that SH-PTP2 is present in axons as well. While immunohistochemistry showed a Nissl-like pattern in large motor neurons, immunoelectron microscopy demonstrated a diffuse pattern of cytoplasmic staining, without apparent preferential localization. The presence of the SH2 domain-containing tyrosine-specific phosphatase SH-PTP2 in diverse neurons in the adult nervous system suggests that SH-PTP2 may play a role in a broad spectrum of neuronal responses. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,LAB CELLULAR NEUROBIOL,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP Reeves, SA (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,NEUROSURG SERV,BOSTON,MA 02129, USA. NR 25 TC 10 Z9 10 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD APR PY 1996 VL 71 IS 4 BP 1037 EP 1042 DI 10.1016/0306-4522(95)00491-2 PG 6 WC Neurosciences SC Neurosciences & Neurology GA UC068 UT WOS:A1996UC06800012 PM 8684607 ER PT J AU Schulz, JB Matthews, RT Henshaw, DR Beal, MF AF Schulz, JB Matthews, RT Henshaw, DR Beal, MF TI Neuroprotective strategies for treatment of lesions produced by mitochondrial toxins: Implications for neurodegenerative diseases SO NEUROSCIENCE LA English DT Article DE Parkinson's disease; Huntington's disease; mitochondria; free radicals; excitotoxicity; coenzyme Q(10) ID EXCITOTOXIC LESIONS; RAT STRIATUM; NEUROTOXICITY; LAMOTRIGINE; IMPAIRMENT; METABOLISM; DISORDERS; PROTECTS; ACID AB Abstraft--Neuronal death in neurodegenerative diseases may involve energy impairment leading to secondary excitotoxicity, and free radical generation. Potential therapies for the treatment of neurodegenerative diseases therefore include glutamate release blockers, excitatory amino acid receptor antagonists, agents that improve mitochondrial function, and free radical scavengers. In the present study we examined whether these strategies either alone or in combination had neuroprotective effects against striatal lesions produced by mitochondrial toxins. The glutamate release blockers lamotrigine and BW1003C87 significantly attenuated lesions produced by intrastriatal administration of 1-melhyl-4-phenylpyridinium. Lamotrigine significantly attenuated lesions produced by systemic administration of 3-nitropropionic acid. Memantine, an N-methyl-D-aspartate antagonist, protected against malonate induced striatal lesions. We previously found that coenzyme Q(10) and nicotinamide, and the free radical spin trap n-tert-butyl-alpha-(2-sulfophenyl)-nitrone (S-PBN) dose-dependently protect against lesions produced by intrastriatal injection of malonate. In the present study we found that the combination of MK-801 (dizocipiline) with coenzyme Q(10) exerted additive neuroprotective effects against malonate. Lamotrigine with coenzyme Q(10) was more effective than coenzyme Q(10) alone. The combination of nictotinamide with S-PBN was more effective than nicotinamide alone. These results provide further evidence that glutamate release inhibitors and N-acetyl-D-aspartate antagonists can protect against secondary excitotoxic lesions in vivo. Furthermore, they show that combinations of agents which act at sequential steps in the neurodegenerative process can produce additive neuroprotective effects. These findings suggest that combinations of therapies to improve mitochondrial function, to block excitotoxicity and to scavenge free radicals may be useful in treating neurodegenerative diseases. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,NEUROCHEM LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RI Schulz, Jorg/D-9786-2012 OI Schulz, Jorg/0000-0002-8903-0593 FU NINDS NIH HHS [NS 10828, NS 31579] NR 28 TC 124 Z9 124 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD APR PY 1996 VL 71 IS 4 BP 1043 EP 1048 DI 10.1016/0306-4522(95)00527-7 PG 6 WC Neurosciences SC Neurosciences & Neurology GA UC068 UT WOS:A1996UC06800013 PM 8684608 ER PT J AU Butler, WE Peterson, JW Zervas, NT Morgan, KG AF Butler, WE Peterson, JW Zervas, NT Morgan, KG TI Intracellular calcium, myosin light chain phosphorylation, and contractile force in experimental cerebral vasospasm SO NEUROSURGERY LA English DT Article DE calcium; cerebral vasospasm; myosin light chain; subarachnoid hemorrhage; vascular tone ID SMOOTH-MUSCLE CELLS; CANINE BASILAR ARTERIES; SUBARACHNOID HEMORRHAGE; CEREBROSPINAL-FLUID; VASCULAR MUSCLE; CA-2+; OXYHEMOGLOBIN; CALMODULIN; KINASE; AEQUORIN AB IT REMAINS UNKNOWN what proportion of delayed arterial narrowing after subarachnoid hemorrhage depends on ongoing metabolic activity within arterial smooth muscle cells versus changes in the passive structural properties of the arterial wall. To determine this, vasospasm was induced by the double subarachnoid hemorrhage model. Anterior spinal artery segments were harvested from control dogs and from dogs with vasospasm. The segments were suspended in a force transducer and stretched to an optimal length for contraction. The difference in tension between 37 and 0 degrees C was defined as the intrinsic tone, and the residual tension at 0 degrees C was defined as the passive tension. The segments taken from dogs with vasospasm had increased intrinsic tone and passive tension (the differences were 3.8 kN/m(2) [P < 0.05] and 14.8 kN/m(2) [P < 0.025], respectively). Hence, the passive component accounted for 79.6% of the increased tension in vasospastic arterial segments. The intracellular calcium concentration was measured in these segments, using the luminescent calcium indicator aequorin. The vasospastic segments had increased basal intracellular calcium concentration (398 versus 258 nmol/L, P < 0.025). In parallel experiments, control and vasospastic vessels were immediately excised when the animals were killed, and the vessels were quick-frozen. Subsequently, using two-dimensional gel electrophoresis to measure percent myosin light chain phosphorylation, vasospastic vessels were found to have increased myosin light chain phosphorylation (37 versus 2%, P < 0.05). The increased intracellular calcium concentration and increased percent myosin light chain phosphorylation in vasospastic segments implicate a role for the Ca2+ dependent pathway of smooth muscle cell contraction in vasospasm. C1 HARVARD UNIV, SCH MED, MASSACHUSETTS GEN HOSP, BOSTON BIOMED RES INST, BOSTON, MA 02114 USA. RP Butler, WE (reprint author), HARVARD UNIV, SCH MED,MASSACHUSETTS GEN HOSP,NEUROSURG SERV, 32 FRUIT ST, ACC 021, BOSTON, MA 02114 USA. NR 46 TC 44 Z9 44 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD APR PY 1996 VL 38 IS 4 BP 781 EP 787 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA UA471 UT WOS:A1996UA47100074 ER PT J AU Cosgrove, GR Buchbinder, BR Jiang, H AF Cosgrove, GR Buchbinder, BR Jiang, H TI Functional magnetic resonance imaging for intracranial navigation SO NEUROSURGERY CLINICS OF NORTH AMERICA LA English DT Article ID CEREBRAL BLOOD-FLOW; CORTEX; STIMULATION; METABOLISM; SYSTEM AB Functional MR imaging can provide accurate anatomic and physiologic localization of human cortical function. This new method of noninvasive cortical mapping appears to be valuable preoperatively for risk assessment, therapeutic decision making and surgical planning. The integrated volume rendering of brain surface topography, cortical veins, structural lesion, and sites of functional activation is also useful intraoperatively for defining cortical resection boundaries in patients with lesions in critical areas. C1 HARVARD UNIV,DEPT RADIOL,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP Cosgrove, GR (reprint author), HARVARD UNIV,DEPT NEUROSURG,MASSACHUSETTS GEN HOSP,SCH MED,15 PARKMAN ST,ACC SUITE 331,BOSTON,MA 02114, USA. NR 16 TC 47 Z9 47 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1042-3680 J9 NEUROSURG CLIN N AM JI Neurosurg. Clin. N. Am. PD APR PY 1996 VL 7 IS 2 BP 313 EP & PG 11 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA UF970 UT WOS:A1996UF97000013 PM 8726444 ER PT J AU Calamante, F Williams, SR vanBruggen, N Kwong, KK Turner, R AF Calamante, F Williams, SR vanBruggen, N Kwong, KK Turner, R TI A model for quantification of perfusion in pulsed labelling techniques SO NMR IN BIOMEDICINE LA English DT Article ID CEREBRAL BLOOD-FLOW; RAT-BRAIN PERFUSION; ARTERIAL WATER; SPIN INVERSION; MR; STIMULATION; SATURATION; T1; T2 AB A model for quantification of perfusion in pulsed labelling techniques is described, based on solving the modified Bloch equation including the effects of flow. The model is designed to fit experimental data acquired in two separate measurements (inversion and control, or selective and non-selective inversions) for different inversion times using a biexponential. Although the signal contrast is 50% less than the continuous labelling technique, it seems more appropriate for human studies because of its lower power deposition, shorter transit time and the use of an interleaved acquisition. The importance is shown of including in the model the difference in relaxation time between blood and tissue. Neglecting this difference can lead to an overestimation of flow, which can be as big as 100% in white matter and 20% in grey matter. C1 INST CHILD HLTH,RCS UNIT BIOPHYS,LONDON WC1N 1EH,ENGLAND. MASSACHUSETTS GEN HOSP,NMR CTR,DEPT RADIOL,CHARLESTOWN,MA 02129. RI Turner, Robert/C-1820-2008 FU Wellcome Trust NR 24 TC 65 Z9 66 U1 0 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0952-3480 J9 NMR BIOMED JI NMR Biomed. PD APR PY 1996 VL 9 IS 2 BP 79 EP 83 DI 10.1002/(SICI)1099-1492(199604)9:2<79::AID-NBM399>3.0.CO;2-4 PG 5 WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy GA VH916 UT WOS:A1996VH91600006 PM 8887372 ER PT J AU Tearney, GJ Boppart, SA Bouma, BE Brezinski, ME Weissman, NJ Southern, JF Fujimoto, JG AF Tearney, GJ Boppart, SA Bouma, BE Brezinski, ME Weissman, NJ Southern, JF Fujimoto, JG TI Scanning single-mode fiber optic catheter-endoscope for optical coherence tomography SO OPTICS LETTERS LA English DT Article AB We describe a new optical coherence tomography catheter-endoscope for micrometer-scale, cross-sectional imaging in internal organ systems. The catheter-endoscope uses single-mode fiber optics with a novel transverse scanning design. The distal end of the catheter-endoscope uses a gradient-index lens with a microprism to emit and collect a single spatial-mode optical beam with specific focusing characteristics. The beam is scanned in a circumferential pattern and can image transverse cross sections through the structure into which it is inserted. A device with a diameter as small as 1.1 mm has been achieved, and imaging of in vitro human venous morphology is demonstrated. (C) 1996 Optical Society of America C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Tearney, GJ (reprint author), MIT,ELECTR RES LAB,DEPT ELECT ENGN & COMP ENGN,CAMBRIDGE,MA 02139, USA. RI Boppart, Stephen/C-7338-2009 NR 14 TC 229 Z9 235 U1 0 U2 15 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 SN 0146-9592 J9 OPT LETT JI Opt. Lett. PD APR 1 PY 1996 VL 21 IS 7 BP 543 EP 545 DI 10.1364/OL.21.000543 PG 3 WC Optics SC Optics GA UC298 UT WOS:A1996UC29800033 PM 19865466 ER PT J AU Collins, JJ Grier, HE Sethna, NF Wilder, RT Berde, CB AF Collins, JJ Grier, HE Sethna, NF Wilder, RT Berde, CB TI Regional anesthesia for pain associated with terminal pediatric malignancy SO PAIN LA English DT Article DE opioids; pain, cancer; pain, neuropathic; pain, pediatric ID CANCER PAIN; ANALGESIA; PATIENT AB The objectives of this study were to identify the characteristics of children who required regional anesthesia for pain associated with terminal malignancy and to identify the safety, tolerability and effectiveness of regional anesthesia as an analgesic modality in terminal pediatric malignancy, A retrospective examination was made of the medical records of children who died of malignancy following treatment at the Dana-Farber Cancer Institute and Children's Hospital, Boston, Massachusetts, and who required either epidural or subarachnoid infusions, or neurolytic blockade for pain management(June, 1986 - April, 1994) during the terminal phase of their illness, Eleven patients were identified, with a duration of epidural or subarachnoid infusions ranging from 3 days to 7 weeks. Indications for this intervention included limiting side effects of opioids, neuropathic pain unresponsive to either rapid escalation of opioids or massive opioid infusions, analgesia for thoracocenteses for the drainage of malignant pleural effusions and instillation of intrapleural chemotherapy. Pain was localized to one area in all patients. Analgesia was judged to be satisfactory in all cases after regional anesthesia was instituted and remained satisfactory in all cases throughout the treatment course, Complications associated with regional anesthesia included dural puncture headache and mild respiratory depression, Five patients were nursed at home with either epidural or subarachnoid infusions, C1 CHILDRENS HOSP,PAIN TREATMENT SERV,BOSTON,MA 02115. CHILDRENS HOSP,DEPT ANESTHESIA,BOSTON,MA 02115. CHILDRENS HOSP,DEPT MED,BOSTON,MA 02115. CHILDRENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. NR 19 TC 39 Z9 40 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD APR PY 1996 VL 65 IS 1 BP 63 EP 69 DI 10.1016/0304-3959(95)00193-X PG 7 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA UV461 UT WOS:A1996UV46100012 PM 8826491 ER PT J AU Insoft, RM Sanderson, IR Walker, WA AF Insoft, RM Sanderson, IR Walker, WA TI Development of immune function in the intestine and its role in neonatal diseases SO PEDIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID FETAL SMALL-INTESTINE; TOXIGENIC ESCHERICHIA-COLI; PLATELET-ACTIVATING FACTOR; ENHANCES IGA PRODUCTION; BIRTH-WEIGHT INFANTS; T-CELL PRODUCT; NECROTIZING ENTEROCOLITIS; HUMAN-MILK; EPITHELIAL-CELLS; PEYERS PATCHES AB The gastrointestinal tract has an essential role in normal immune function. The ontogeny and physiology of neonatal gut immunity are discussed. Because the gastrointestinal tract serves as the portal of entry for many potential antigens, breakdown in mucosal defense mechanisms could lead to potentially life-threatening conditions, such as necrotizing enterocolitis, milk-protein enteropathy, and intestinal infections. Proposed immune-mediated mechanisms and possible treatments for these conditions are reviewed. C1 MASSACHUSETTS GEN HOSP, COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR, DEV GASTROENTEROL LAB, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. CHILDRENS HOSP, BOSTON, MA USA. RP Insoft, RM (reprint author), MASSACHUSETTS GEN HOSP, DIV NEONATOL, DEPT PEDIAT, FOUNDERS HOUSE 442, FRUIT ST, BOSTON, MA 02114 USA. FU NICHD NIH HHS [HD-12437, HD-31812]; NIDDK NIH HHS [P01-DK-33506] NR 83 TC 75 Z9 78 U1 1 U2 4 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0031-3955 EI 1557-8240 J9 PEDIATR CLIN N AM JI Pediatr. Clin. N. Am. PD APR PY 1996 VL 43 IS 2 BP 551 EP + DI 10.1016/S0031-3955(05)70420-X PG 0 WC Pediatrics SC Pediatrics GA UF542 UT WOS:A1996UF54200014 PM 8614615 ER PT J AU Winter, H Chang, TL AF Winter, H Chang, TL TI Gastrointestinal and nutritional problems in children with immunodeficiency and AIDS SO PEDIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID VIRUS-INFECTION; CHRONIC DIARRHEA; BODY-COMPOSITION; HIV-INFECTION; TYPE-1; TRANSMISSION; ZIDOVUDINE; SYMPTOMS; SURVIVAL; DISEASE AB Gastrointestinal and nutritional problems of children with primary and secondary immunodeficiency syndromes are reviewed. Pathobiology, clinical manifestations, and issues relating to nutrient utilization and requirements are discussed. The gastrointestinal manifestations of HIV disease in children during the progression from acquisition of virus to AIDS are correlated with changes in systemic immune function and with environmental and social factors that have impact on the severity of disease. C1 BOSTON CITY HOSP,DIV PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02118. CHILDRENS HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP Winter, H (reprint author), BOSTON UNIV,SCH MED,DIV PEDIAT GASTROENTEROL & NUTR,801 ALBANY ST,S-117,BOSTON,MA 02118, USA. NR 40 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0031-3955 J9 PEDIATR CLIN N AM JI Pediatr. Clin. N. Am. PD APR PY 1996 VL 43 IS 2 BP 573 EP & DI 10.1016/S0031-3955(05)70421-1 PG 19 WC Pediatrics SC Pediatrics GA UF542 UT WOS:A1996UF54200015 PM 8614616 ER PT J AU Khurana, DS Bonnemann, CG Dooling, EC Ouellette, EM Buonanno, F AF Khurana, DS Bonnemann, CG Dooling, EC Ouellette, EM Buonanno, F TI Vertebral artery dissection: Issues in diagnosis and management SO PEDIATRIC NEUROLOGY LA English DT Article ID VERTEBROBASILAR OCCLUSIVE DISEASE; CHILDREN; INFARCTION; CHILDHOOD; TRAUMA AB Vertebral artery dissection is an uncommon cause of stroke in children, Accuracy of diagnosis by magnetic resonance angiography (MRA) instead of invasive transfemoral angiography (TFA) has been controversial, The need for anticoagulation and duration of such therapy is also arguable, We report 2 boys with vertebral artery dissection: one, aged 7 years, presented with hemiparesis and seizures and the other, aged 4 years,presented with ataxia. Each boy's initial MRA was not interpreted as delineating occlusive lesions to explain the posterior circulation infarcts visualized on computed tomography and magnetic resonance imaging scans, However, subsequent MRAs were suspicious for vertebral artery dissection, which was confirmed by TFA, Both children were treated with anticoagulation therapy. The first patient continued to manifest evidence of new infarcts despite treatment (initially with aspirin alone, followed by anticoagulation with heparin and warfarin), and is now maintained on a combination of high dose warfarin and aspirin, The second patient is now maintained on aspirin alone after initial anticoagulation for 6 months with heparin followed by warfarin, A high index of suspicion for vertebral artery dissection may allow diagnosis on the basis of MRA alone, Previous reports have indicated good outcomes of vertebral artery dissection in children and adults irrespective of anticoagulation treatment, Our experience suggests that anticoagulation may be beneficial in preventing further strokes caused by the dissection. C1 MASSACHUSETTS GEN HOSP,PEDIAT NEUROL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NR 18 TC 29 Z9 30 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0887-8994 J9 PEDIATR NEUROL JI Pediatr. Neurol. PD APR PY 1996 VL 14 IS 3 BP 255 EP 258 DI 10.1016/0887-8994(96)00015-X PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA UM992 UT WOS:A1996UM99200015 PM 8736412 ER PT J AU Castillo, L Beaumier, L Yu, YM Young, VR AF Castillo, L Beaumier, L Yu, YM Young, VR TI Splanchnic uptake and oxidation of proline in healthy subjects. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PEDIAT INTENS CARE UNIT,BOSTON,MA 02114. MIT,HUMAN NUTR LAB,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 255 EP 255 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23800254 ER PT J AU Roberts, JD Bloch, KD AF Roberts, JD Bloch, KD TI Alternate splicing of the vascular endothelial growth factor mRNA is modulated during lung development. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIOVASC RES CTR,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 386 EP 386 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23800386 ER PT J AU Cunniff, C Kratz, LE Moser, A Natowicz, MR Kelley, RI AF Cunniff, C Kratz, LE Moser, A Natowicz, MR Kelley, RI TI Clinical spectrum of patients with RSH/Smith-Lemli-Optiz syndrome. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV ARIZONA,DEPT PEDIAT,TUCSON,AZ 85721. UNIV ARIZONA,STEELE MEM CHILDRENS RES CTR,TUCSON,AZ 85721. KENNEDY KRIEGER INST,BALTIMORE,MD. JOHNS HOPKINS UNIV,BALTIMORE,MD. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,WALTHAM,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 474 EP 474 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23800474 ER PT J AU Boepple, PA Sluss, PM Khoury, R Crowley, WF AF Boepple, PA Sluss, PM Khoury, R Crowley, WF TI Follistatin (FS) and inhibin A & B in central precocious puberty (CPP): Impact of GnRH agonist (GnRHa)-induced pituitary desensitization. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT UNIT,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,REPROD ENDOCRINE UNIT,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 491 EP 491 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23800491 ER PT J AU Capriles, C Grinstein, G Boepple, PA Crawford, JD Lee, MM Levitsky, LL AF Capriles, C Grinstein, G Boepple, PA Crawford, JD Lee, MM Levitsky, LL TI Ambiguous diagnosis: Adrenal suppression in congenital adrenal hyperplasia (CAH). SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT SERV,PEDIAT ENDOCRINOL UNIT,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 497 EP 497 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23800497 ER PT J AU Lee, MM Gustafson, ML Silverman, BL Hasegawa, T Hasegawa, Y Donahoe, PK MacLaughlin, DT AF Lee, MM Gustafson, ML Silverman, BL Hasegawa, T Hasegawa, Y Donahoe, PK MacLaughlin, DT TI Mullerian inhibiting substance (MIS) determination in the evaluation of nonpalpable gonads. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT ENDO UNIT,BOSTON,MA. NORTHWESTERN UNIV,SCH MED,DIV PEDIAT ENDO,CHICAGO,IL. CHILDRENS MEM HOSP,CHICAGO,IL 60614. TOKYO METROPOLITAN KIYOSE CHILDRENS HOSP,DIV ENDOCRINOL & METAB,TOKYO,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 534 EP 534 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23800535 ER PT J AU Barlow, S Kaplan, S Khan, A Sullivan, L Danford, D Cutler, L Parsons, S Greenfield, S Grand, R AF Barlow, S Kaplan, S Khan, A Sullivan, L Danford, D Cutler, L Parsons, S Greenfield, S Grand, R TI Clinical severity scale development in pediatric chronic disease. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV NEBRASKA,LINCOLN,NE 68583. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. DANA FARBER CANC INST,BOSTON,MA 02115. PRIMARY CARE OUTCOMES RES INST,BOSTON,MA. TUFTS UNIV,NEW ENGLAND MED CTR,BOSTON,MA 02111. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 764 EP 764 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23800765 ER PT J AU Chang, E Boyd, AJ Nelson, CC Crowley, D Ezekowitz, RAB Castle, VP AF Chang, E Boyd, AJ Nelson, CC Crowley, D Ezekowitz, RAB Castle, VP TI Successful treatment of complicated childhood hemangiomas with interferon alpha 2B SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 UNIV MICHIGAN,MED CTR,DEPT PEDIAT,ANN ARBOR,MI 48109. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 908 EP 908 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23800908 ER PT J AU Cooke, KR Martin, TR Kobzik, L Brewer, J Delmonte, J Ferrara, JLM AF Cooke, KR Martin, TR Kobzik, L Brewer, J Delmonte, J Ferrara, JLM TI The roles of alloreactivity and endotoxin in an experimental model of idiopathic pneumonia syndrome after bone marrow transplantation. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,BOSTON,MA. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV RESP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 909 EP 909 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23800909 ER PT J AU Kupfer, GM DAndrea, AD AF Kupfer, GM DAndrea, AD TI The Fanconi anemia polypeptide, FAC, normalizes p53 induction in a transfected hematopoietic cell line SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL & CELLULAR MOL BIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 930 EP 930 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23800930 ER PT J AU KurtJones, EA Thompson, C Novitsky, T Siber, G Fleisher, G AF KurtJones, EA Thompson, C Novitsky, T Siber, G Fleisher, G TI Endotoxin neutralizing protein inhibits the response of human peripheral blood mononuclear cells to LPS and non-LPS stimuli. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,CHILDRENS HOSP,MED CTR,SCH MED,DEPT PEDIAT,DIV EMERGENCY MED,BOSTON,MA 02115. DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. ASSOCIATES CAPE COD INC,WOODS HOLE,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 1045 EP 1045 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23801045 ER PT J AU Malley, R Stack, AM Thompson, CM Ferretti, ML Siber, GR Fleisher, GR Saladino, RA AF Malley, R Stack, AM Thompson, CM Ferretti, ML Siber, GR Fleisher, GR Saladino, RA TI An infant rat model of Streptococcus pneumoniae (SP) nasal colonization and invasive pneumococcal disease. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP,DIV EMERGENCY MED,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 1054 EP 1054 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23801054 ER PT J AU Malley, R Thompson, CM Ferretti, ML Siber, GR Saladino, RA AF Malley, R Thompson, CM Ferretti, ML Siber, GR Saladino, RA TI Bacterial polysaccharide immune globulin (BPIG) does not protect infant rats from nasal colonization with Streptococcus pneumoniae (SP). SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP,DIV EMERGENCY MED,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 1055 EP 1055 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23801055 ER PT J AU Modlin, JF Bergelson, JM WielandAlter, W Finberg, RW AF Modlin, JF Bergelson, JM WielandAlter, W Finberg, RW TI Group B coxsackieviruses (CBV) use both decay accelerating factor and a 50 KD protein as receptors. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 DARTMOUTH COLL SCH MED,DEPT PEDIAT,LEBANON,NH. DARTMOUTH COLL SCH MED,DEPT MED,LEBANON,NH. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 1064 EP 1064 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23801064 ER PT J AU Modlin, JF Bergelson, JM WielandAlter, W Finberg, RW AF Modlin, JF Bergelson, JM WielandAlter, W Finberg, RW TI A monoclonal antibody to decay accelerating factor (DAF) prevents in vitro infection by several echovirus serotypes. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 DARTMOUTH COLL SCH MED,DEPT PEDIAT,LEBANON,NH. DARTMOUTH COLL SCH MED,DEPT MED,LEBANON,NH. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 1065 EP 1065 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23801065 ER PT J AU Saladino, RA Stack, AM Thompson, CM Fleisher, GR Siber, GR AF Saladino, RA Stack, AM Thompson, CM Fleisher, GR Siber, GR TI Infant rat model of vaccine type S-pneumoniae (SP) pneumonia. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP,DIV EMERGENCY MED,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. DANA FARBER CANC INST,DIV INFECT DIS,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 1091 EP 1091 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23801091 ER PT J AU Saladino, RA Stack, AM Malley, R Thompson, CM Siber, GR Fleisher, GR AF Saladino, RA Stack, AM Malley, R Thompson, CM Siber, GR Fleisher, GR TI Bacterial polysaccharide immune globulin (BPIG) protects infants rats with S-pneumoniae (SP) pneumonia from bacteremia, meningitis and death. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP,DIV EMERGENCY MED,BOSTON,MA. DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 1092 EP 1092 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23801092 ER PT J AU Weiner, DL Heney, D Bailey, CC Lewis, IJ Ezekowitz, RAB AF Weiner, DL Heney, D Bailey, CC Lewis, IJ Ezekowitz, RAB TI In vivo analysis reveals a role for human mannose-binding protein in acute sepsis. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP,BOSTON,MA. ST JAMES HOSP,LEEDS LS9 7TF,W YORKSHIRE,ENGLAND. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 1113 EP 1113 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23801113 ER PT J AU Roberts, JD Fineman, J Morin, FC Shaul, PW Rimar, S Schreiber, MD Polin, RA Thusu, KG Zayek, M Zwass, MS Zellers, TM Wylam, ME Gross, I Zapol, WM Heymann, MA AF Roberts, JD Fineman, J Morin, FC Shaul, PW Rimar, S Schreiber, MD Polin, RA Thusu, KG Zayek, M Zwass, MS Zellers, TM Wylam, ME Gross, I Zapol, WM Heymann, MA TI Inhaled nitric oxide gas improves oxygenation in PPHN. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CAMBRIDGE,MA 02138. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. SUNY BUFFALO,BUFFALO,NY 14260. UNIV TEXAS,SW MED CTR,DALLAS,TX 75235. YALE UNIV,NEW HAVEN,CT 06520. CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 1430 EP 1430 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23801431 ER PT J AU Catlin, EA Teixeira, J Tonnu, VC Ebb, RG Pacheco, BA Manganaro, TF AF Catlin, EA Teixeira, J Tonnu, VC Ebb, RG Pacheco, BA Manganaro, TF TI Mullerian inhibiting substance in branching morphogenesis of fetal lung. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 1952 EP 1952 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23801952 ER PT J AU Brem, AS Bina, RB Ingelfinger, JR AF Brem, AS Bina, RB Ingelfinger, JR TI Glucocorticoids mediate angiotensin II (ang II) induced electrolyte: Transport in immortalized renal proximal tubule cells (IRPTC). SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 RHODE ISL HOSP,DIV PEDIAT NEPHROL,PROVIDENCE,RI 02902. MASSACHUSETTS GEN HOSP,DIV PEDIAT NEPHROL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 2134 EP 2134 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23802133 ER PT J AU Ingelfinger, JR Haveran, L Diamant, D Jung, FF Tang, SS AF Ingelfinger, JR Haveran, L Diamant, D Jung, FF Tang, SS TI Angiotensin II (ANG II) modulates response to oxidant injury in immortalized rat proximal tubule cells (IRPTC). SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PEDIAT NEPHROL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 2157 EP 2157 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23802156 ER PT J AU Norling, LL Smith, RM Ingelfinger, JR AF Norling, LL Smith, RM Ingelfinger, JR TI Stored and secreted rat kidney renin isoforms differ in molecular weight and isoelectric point. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT NEPHROL UNIT,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1996 VL 39 IS 4 BP 2179 EP 2179 PN 2 PG 1 WC Pediatrics SC Pediatrics GA UD238 UT WOS:A1996UD23802178 ER PT J AU Gonzalez, S Pathak, MA AF Gonzalez, S Pathak, MA TI Inhibition of ultraviolet-induced formation of reactive oxygen species, lipid peroxidation, erythema and skin photosensitization by Polypodium leucotomos SO PHOTODERMATOLOGY PHOTOIMMUNOLOGY & PHOTOMEDICINE LA English DT Article DE ultraviolet radiation; lipid peroxidation; reactive oxygen species; erythema; photosensitization; Polypodium leucotomos ID ARACHIDONIC-ACID; INDUCED DAMAGE; RADIATION; IRRADIATION; PSORALENS; CALAGUALA AB The acute reactions of human skin to solar ultraviolet radiation (290-400 nm) are recognized as a form of inflammation reactions that are mediated by several possible mechanisms including (a) direct action of photons on DNA, (b) generation of reactive free radicals and reactive oxygen species involving the formation of O-2(.-), O-1(2), H2O2, (OH)-O-., etc., (c) generation of prostaglandins (PCD2, PGE(2), etc.), histamine, leucotrienes, and other inflammatory mediators. It is conceivable that UV-induced reactions represent oxidative stress mediated by the formation of free radicals, reactive oxygen, lipid peroxidation, liberation of membrane phospholipids, and subsequent formation of prostaglandins by cyclo-oxygenase pathway. In this study, we examined the role of reactive oxygen species and lipid peroxidation in in vitro reactions as well as in vivo skin inflammation reactions induced by (a) UVB radiation (290-320 nm), and (b) skin photosensitization reaction by PUVA treatment involving 8-methoxypsoralen and UVA (320-400 nm) radiation and presented data for the generation of superoxide anion (O-2(.-)) and lipid peroxides. We have also evaluated, both in vitro as well as in vivo systems, the quenching or the inhibition of O-2(.-) by a plant extract known as Polypodium leucotomos. The P. leucotomos extract was found to exhibit interesting antioxidant and anti-inflammatory as well as photoprotective properties against photo-oxidative stress involving the generation of reactive oxygen, lipid peroxidation under in vitro reactions as well as in vivo experimental conditions. Significant inhibition of UVB-induced erythemal response, and 8-methoxypsoralen plus UVA-induced phototoxic reaction after topical application or oral administration of the photosensitizer could be demonstrated in guinea pig skin and human skin following the topical application of P. leucotomos extract. The photoprotective mechanism of P. leucotomos involving interaction with reactive oxygen species or free radicals appears to have potential clinical usefulness in preventing sunburn and inhibiting phototoxic reaction. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. FU NCI NIH HHS [5-RO1-CA-05003-34] NR 38 TC 69 Z9 74 U1 0 U2 4 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0905-4383 J9 PHOTODERMATOL PHOTO JI Photodermatol. Photoimmunol. Photomed. PD APR PY 1996 VL 12 IS 2 BP 45 EP 56 PG 12 WC Dermatology SC Dermatology GA VL400 UT WOS:A1996VL40000001 PM 8897589 ER PT J AU Gonzalez, S Hegyi, V Baqer, A Sadiq, I Kollias, N AF Gonzalez, S Hegyi, V Baqer, A Sadiq, I Kollias, N TI Development of cutaneous tolerance to ultraviolet B during ultraviolet B phototherapy for psoriasis SO PHOTODERMATOLOGY PHOTOIMMUNOLOGY & PHOTOMEDICINE LA English DT Article DE ultraviolet B; tolerance; accommodation; psoriasis; phototherapy; skin; chronic exposure ID SOLAR URTICARIA; UV-B; HUMAN-SKIN; PYRIMIDINE DIMERS; RADIATION; PHOTOCHEMOTHERAPY; REPAIR; INVIVO; DNA AB During a schedule of multiple exposures to ultraviolet B radiation (UVB, 280-320 nm), skin develops a reduced sensitivity, variously called tolerance, photoadaptation, accomodation or acclimatization. In this study we have investigated the development of tolerance in the normal skin of a group of psoriatic patients during the course of UVB therapy. Tolerance was assessed by phototests carried out on non-lesional skin as frequently as possible throughout the treatment. Maximum tolerance was developed by the group of individuals most sensitive to UVB, which was twice that of the least sensitive group. The minimal perceptible erythema dose (MPE) increased rapidly in the first 2 weeks (220% per week) and reached a plateau by the eighth week of 800% above the baseline MPE dose. For the more sensitive patients there was a further increase in sensitivity (decrease in MPE dose) after the ninth week of continuous treatment. Tolerance to UVB also involves pigmentation in the first few weeks, but in these patients there was no evidence of hyperpigmentation by the end of treatment. While epidermal hyperplasia is most likely to play a leading role in the development of tolerance to UV, there is no reason to expect this protection to decrease under conditions of continuous exposure. Thus, accommodation to ultraviolet radiation (UVR) is not a monotonically increasing process but appears to alter the accepted reactions of human skin to UVR. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 33 TC 10 Z9 10 U1 1 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0905-4383 J9 PHOTODERMATOL PHOTO JI Photodermatol. Photoimmunol. Photomed. PD APR PY 1996 VL 12 IS 2 BP 73 EP 78 PG 6 WC Dermatology SC Dermatology GA VL400 UT WOS:A1996VL40000004 PM 8897592 ER PT J AU DAmbra, M AF DAmbra, M TI Perioperative epoetin alfa reduces transfusion requirements in coronary artery bypass graft surgery SO SEMINARS IN HEMATOLOGY LA English DT Article; Proceedings Paper CT Roundtable of Experts in Surgery Blood Management CY APR 07-09, 1995 CL VIENNA, AUSTRIA SP Janssen Cilag, New Brunswick ID MORTALITY RP DAmbra, M (reprint author), MASSACHUSETTS GEN HOSP,FRUIT ST,BOSTON,MA 02114, USA. NR 5 TC 6 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0037-1963 J9 SEMIN HEMATOL JI Semin. Hematol. PD APR PY 1996 VL 33 IS 2 SU 2 BP 73 EP 74 PG 2 WC Hematology SC Hematology GA UH798 UT WOS:A1996UH79800019 ER PT J AU Callahan, RJ AF Callahan, RJ TI The role of commercial nuclear pharmacy in the future practice of nuclear medicine SO SEMINARS IN NUCLEAR MEDICINE LA English DT Article AB It has been estimated that today 70% to 80% of all radiopharmaceutical doses are dispensed through commercial nuclear pharmacy channels. These services are provided by the approximately 250 facilities in the United States, with some multisite corporations dispensing in excess of 20,000 unit dose prescriptions per day. As pressures mount within health care institutions to reduce manpower, increase cost-effectiveness, increase participation in managed care contracts, and to seek outside vendors for many services that were previously provided in-house, the future role of the commercial nuclear pharmacy in the practice of nuclear medicine will only continue to increase. The essence of nuclear pharmacy practice is the dispensing of a full range of high quality radiopharmaceuticals in patient specific unit doses. These doses must be delivered in a timely and cost effective manner, without compromising quality or patient safety. Commercial nuclear pharmacies have expanded to provide such varied functions as radiation safety and waste management, as well as consultative and marketing activities directed towards clinicians within a nuclear medicine practitioners own facility. In service continuing education programs directed towards physicians and technologists are frequently offered by many commercial nuclear pharmacies. Changes in health care economics, merging and down-sizing in the hospital industry, and the overall impact of managed care on the viability of hospitals in general has resulted in slow growth, or even a small decline in the number of institutionally based nuclear pharmacists. As a result, nuclear medicine practitioners will be looking to the commercial nuclear pharmacies to meet a larger portion of their radiopharmaceutical needs, as well as to value added services, such as education and research and development. Specialized practice settings, such as nuclear cardiology and free-standing nuclear medicine clinics, are especially well suited to the services provided by commercial nuclear pharmacies. Involvement in the distribution of positron-emission tomography radiopharmaceuticals will continue to increase regardless of the results of current regulatory debates on this issue. In the future, nuclear medicine practitioners will look to the commercial nuclear pharmacies for an increasing portion of their radiopharmaceutical needs and the industry should be ready and able to meet these demands in a safe, timely, and cost efficient manner. Copyright (C) 1996 by W.B. Saunders Company. RP Callahan, RJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV NUCL MED,55 FRUIT ST,BOSTON,MA 02114, USA. NR 4 TC 3 Z9 3 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0001-2998 J9 SEMIN NUCL MED JI Semin. Nucl. Med. PD APR PY 1996 VL 26 IS 2 BP 85 EP 90 DI 10.1016/S0001-2998(96)80029-8 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA UG731 UT WOS:A1996UG73100003 PM 8723502 ER PT J AU Ruprecht, RM Baba, TW Li, A Ayehunie, S Hu, YW Liska, V Rasmussen, R Sharma, PL AF Ruprecht, RM Baba, TW Li, A Ayehunie, S Hu, YW Liska, V Rasmussen, R Sharma, PL TI Live attenuated HIV as a vaccine for AIDS: Pros and cons SO SEMINARS IN VIROLOGY LA English DT Article DE attenuated live retrovirus vaccines; avirulent viruses; correlates of retroviral immunity; replication-impaired viruses; threshold hypothesis ID VIRUS-INDUCED ERYTHROLEUKEMIA; INDEPENDENT DOWN-REGULATION; CELL-SURFACE CD4; IMMUNODEFICIENCY VIRUS; NEF GENE; RETROVIRUS; IMMUNIZATION; MACAQUES; LEUKEMIA; DISEASE AB Anti-HIV-1 vaccines must be safe and effective. In macaques, live attenuated simian immunodeficiency viruses have provided the best protection to date. Similar results were obtained earlier in murine leukemia virus systems in which protection correlated with cellular immunity but not with neutralizing antibodies. Attenuated primate lentiviruses tested thus far have been replication-impaired but may still harbor genetic determinants encoding virulence. Other safety issues concern insertional oncogenesis, genetic instability, vertical transmission and differential pathogenicity in adults and newborns, and viral persistence with possible reactivation during intercurrent illness. Long term safety studies are needed to assess the risks associated with live attenuated retrovirus vaccines. (C)1996 Academic Press Ltd C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. TUFTS UNIV,SCH MED,DEPT NEWBORN MED,BOSTON,MA 02111. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. RP Ruprecht, RM (reprint author), DANA FARBER CANC INST,LAB VIRAL PATHOGENESIS,BOSTON,MA 02115, USA. NR 51 TC 8 Z9 8 U1 1 U2 3 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 1044-5773 J9 SEMIN VIROL JI Semin. Virol. PD APR PY 1996 VL 7 IS 2 BP 147 EP 155 DI 10.1006/smvy.1996.0019 PG 9 WC Virology SC Virology GA UF923 UT WOS:A1996UF92300009 ER PT J AU Ubel, PA Loewenstein, G AF Ubel, PA Loewenstein, G TI Distributing scarce livers: The moral reasoning of the general public SO SOCIAL SCIENCE & MEDICINE LA English DT Article DE transplantation; equity; prognosis; ethics; health policy ID COST-EFFECTIVENESS ANALYSIS; HEALTH-CARE; POINT SYSTEM; OREGON; RETRANSPLANTATION; EFFICACY AB The transplant system has been criticized for not paying enough attention to efficiency in distributing scarce organs. But little research has been done to see how the general public views tradeoffs between efficiency and equity. We surveyed members of the general public to see how they would distribute organs among patients with varying chances of benefiting from them. In addition, we asked subjects to explain their decisions and to tell us about any other information they would have liked in order to make the decisions. We found that the public places a very high value on giving everyone a chance at receiving scarce resources, even if that means a significant decrease in the chance that available organs will save people's lives. Our results raise important questions about whether the aims of outcomes research and cost-effective studies agree with the values of the general public. C1 UNIV PENN,DIV GEN INTERNAL MED,PHILADELPHIA,PA 19104. UNIV PENN,CTR BIOETH,PHILADELPHIA,PA 19104. UNIV PENN,LEONARD DAVIS INST HLTH ECON,PHILADELPHIA,PA 19104. CARNEGIE MELLON UNIV,DEPT SOCIAL & DECIS SCI,PITTSBURGH,PA 15213. RP Ubel, PA (reprint author), VET AFFAIRS MED CTR,PHILADELPHIA,PA, USA. NR 27 TC 71 Z9 72 U1 2 U2 7 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0277-9536 J9 SOC SCI MED JI Soc. Sci. Med. PD APR PY 1996 VL 42 IS 7 BP 1049 EP 1055 DI 10.1016/0277-9536(95)00216-2 PG 7 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA UD561 UT WOS:A1996UD56100009 PM 8730910 ER PT J AU McGovern, BA Liberthson, R AF McGovern, BA Liberthson, R TI Arrhythmias induced by exercise in athletes and others SO SOUTH AFRICAN MEDICAL JOURNAL LA English DT Article ID RADIOFREQUENCY CATHETER ABLATION; PARKINSON-WHITE SYNDROME; SUDDEN-DEATH; RHODE-ISLAND AB Athletes are subject to the same arrhythmias as the general population, but the frequency and significance of the arrhythmias may be different. Cardiovascular conditioning slows the heart rate and may make athletes more vulnerable to neurocardiogenic syncope and atrial fibrillation. Tachyarrhythmias may be precipitated by vigorous exercise and more severe rate-related symptoms may result because of the high sympathetic drive during sports activities. For those with pre-existing cardiovascular abnormalities, athletic activity may be beneficial in some cases, but dangerous and even life-threatening in others. A review of the subject and recommendations based on our personal experience and a recent consensus conference are provided. RP McGovern, BA (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114, USA. NR 22 TC 8 Z9 8 U1 0 U2 2 PU MED ASSOC S AFRICA PI JOHANNESBURG PA MED HOUSE CENTRAL SQ 7430 PINELANDS JOHANNESBURG, SOUTH AFRICA SN 0038-2469 J9 S AFR MED J JI S. Afr. Med. J. PD APR PY 1996 VL 86 SU 2 BP C78 EP C82 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA VJ326 UT WOS:A1996VJ32600004 PM 8711581 ER PT J AU Ayata, C Moskowitz, MA AF Ayata, C Moskowitz, MA TI Ketamine antagonizes nitric oxide release from cerebral cortex after middle cerebral artery ligation in rats - Editorial comment SO STROKE LA English DT Editorial Material RP Ayata, C (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA, USA. RI Moskowitz, Michael/D-9916-2011 NR 5 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD APR PY 1996 VL 27 IS 4 BP 752 EP 752 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA UD834 UT WOS:A1996UD83400039 ER PT J AU Grossbard, ML AF Grossbard, ML TI Is laparoscopic splenectomy appropriate for the management of hematologic and oncologic diseases? SO SURGICAL ENDOSCOPY-ULTRASOUND AND INTERVENTIONAL TECHNIQUES LA English DT Editorial Material ID CLINICAL STAGE-I; HODGKINS-DISEASE RP Grossbard, ML (reprint author), MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,COX 315,100 BLOSSOM ST,BOSTON,MA 02114, USA. NR 12 TC 23 Z9 23 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0930-2794 J9 SURG ENDOSC-ULTRAS JI Surg. Endosc.-Ultrason. Interv. Tech. PD APR PY 1996 VL 10 IS 4 BP 387 EP 388 DI 10.1007/BF00191620 PG 2 WC Surgery SC Surgery GA UD837 UT WOS:A1996UD83700002 PM 8661783 ER PT J AU Samuels, MH Kramer, P AF Samuels, MH Kramer, P TI Effects of metoclopramide on fasting-induced TSH suppression SO THYROID LA English DT Article ID THYROTROPIN-RELEASING-HORMONE; DOPAMINERGIC ACTIVITY; SERUM THYROTROPIN; MALE-RATS; SECRETION; STARVATION; PROLACTIN AB Short-term caloric deprivation leads to suppression of TSH secretion in healthy subjects, but the mechanism of this effect is unknown. Since dopamine inhibits TSH secretion at physiologic levels, increased endogenous dopamine activity may cause the TSH suppression observed during fasting. To test this hypothesis, 11 healthy subjects underwent four studies: (1) Baseline-subjects were allowed ad libitum food. (2) MCP-subjects were allowed ad libitum food and received iv metoclopramide (MCP) at 30 mu g/kg/h over 48 h. (3) Easting-subjects received no caloric intake for 56 h. (4) Fasting + MCP-subjects fasted for 56 h, and received iv MCP during the final 48 h of the study. Serum TSH levels were measured every 15 min during the final 24 h of each study, and a TRH stimulation test was performed at the conclusion of each study: 56 h of fasting decreased 24 h mean TSH levels and TSH pulse amplitude by 40%, with blunting of the TSH response to TRH. MCP infusions increased 24 h mean TSH levels and TSH pulse amplitude 26-34%, with no differences between the fasting and nonfasting studies. MCP infusions did not normalize TSH levels, TSH responses to TRH, or serum T-3 levels during fasting. These data suggest that endogenous dopaminergic activity does not play a major role in fasting-induced TSH suppression in healthy subjects. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 77030. RP Samuels, MH (reprint author), OREGON HLTH SCI UNIV,DIV ENDOCRINOL,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. FU NCRR NIH HHS [M01-RR-00334, M01-RR-00051] NR 25 TC 5 Z9 7 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD APR PY 1996 VL 6 IS 2 BP 85 EP 89 DI 10.1089/thy.1996.6.85 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UJ989 UT WOS:A1996UJ98900004 PM 8733877 ER PT J AU McMorrow, IM Comrack, C Sachs, DH Monroy, R DerSimonian, H AF McMorrow, IM Comrack, C Sachs, DH Monroy, R DerSimonian, H TI Characterization of the human alpha 1,3Gal-reactive natural antibody population SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 3rd International Congress for Xenotransplantation CY SEP 27-OCT 01, 1995 CL BOSTON, MA C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. BIOTRANSPLANT INC,BOSTON,MA. NR 5 TC 6 Z9 6 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1996 VL 28 IS 2 BP 547 EP 547 PG 1 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA UG383 UT WOS:A1996UG38300012 PM 8623259 ER PT J AU Yang, YG Glaser, RM Monroy, R Swenson, K Sykes, M AF Yang, YG Glaser, RM Monroy, R Swenson, K Sykes, M TI Enhanced porcine hematopoiesis in mice receiving donor-specific interleukin-3 SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 3rd International Congress for Xenotransplantation CY SEP 27-OCT 01, 1995 CL BOSTON, MA C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,SURG SERV,BOSTON,MA 02129. FU NHLBI NIH HHS [R01 HL49915] NR 3 TC 3 Z9 3 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1996 VL 28 IS 2 BP 655 EP 655 PG 1 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA UG383 UT WOS:A1996UG38300081 PM 8623328 ER PT J AU Gritsch, HA Sykes, M AF Gritsch, HA Sykes, M TI Hematopoietic competition limits xenogeneic myeloid reconstitution in SCID mice SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 3rd International Congress for Xenotransplantation CY SEP 27-OCT 01, 1995 CL BOSTON, MA ID BARRIER C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. FU PHS HHS [R01 49915] NR 5 TC 3 Z9 3 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1996 VL 28 IS 2 BP 708 EP 708 PG 1 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA UG383 UT WOS:A1996UG38300110 PM 8623357 ER PT J AU Banerjee, PT Ierino, F Kaynor, GC Giovino, M Sablinski, T Emery, DW Rosa, MD LeGuern, C Sachs, DH Monroy, RL AF Banerjee, PT Ierino, F Kaynor, GC Giovino, M Sablinski, T Emery, DW Rosa, MD LeGuern, C Sachs, DH Monroy, RL TI Retrovirus-mediated transfer and expression of swine MHC class II genes in CD34(+) monkey stem cells SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 3rd International Congress for Xenotransplantation CY SEP 27-OCT 01, 1995 CL BOSTON, MA ID MINIATURE SWINE C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02114. RP Banerjee, PT (reprint author), BIOTRANSPLANT INC,75 3RD AVE,BOSTON,MA 02129, USA. NR 5 TC 7 Z9 7 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1996 VL 28 IS 2 BP 747 EP 748 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA UG383 UT WOS:A1996UG38300131 PM 8623378 ER PT J AU Yamada, K DerSimonian, H Sachs, DH AF Yamada, K DerSimonian, H Sachs, DH TI The mechanism of xenogeneic cell-mediated lympholysis between human and pig cells SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 3rd International Congress for Xenotransplantation CY SEP 27-OCT 01, 1995 CL BOSTON, MA C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. NR 1 TC 1 Z9 1 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1996 VL 28 IS 2 BP 757 EP 757 PG 1 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA UG383 UT WOS:A1996UG38300136 PM 8623383 ER PT J AU Powelson, J Bailin, M Bartholomew, A Boskebick, S Colvin, R Hong, HZ Johnson, M Kimikawa, M Sablinski, T Wee, SL Sachs, D Cosimi, AB AF Powelson, J Bailin, M Bartholomew, A Boskebick, S Colvin, R Hong, HZ Johnson, M Kimikawa, M Sablinski, T Wee, SL Sachs, D Cosimi, AB TI A mixed chimerism approach to renal transplantation between concordant nonhuman primate species SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 3rd International Congress for Xenotransplantation CY SEP 27-OCT 01, 1995 CL BOSTON, MA C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. RP Powelson, J (reprint author), MASSACHUSETTS GEN HOSP,BLAKE 655,FRUIT ST,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-18646] NR 1 TC 6 Z9 6 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1996 VL 28 IS 2 BP 761 EP 761 PG 1 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA UG383 UT WOS:A1996UG38300140 PM 8623387 ER PT J AU Paguio, CG Germana, S LeGuern, C Jubinsky, P Sachs, DH Emery, DW AF Paguio, CG Germana, S LeGuern, C Jubinsky, P Sachs, DH Emery, DW TI Derivation of immortalized swine stromal cell lines SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 3rd International Congress for Xenotransplantation CY SEP 27-OCT 01, 1995 CL BOSTON, MA C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA. FU NHLBI NIH HHS [1 R01 HL54038, 5 R01 HL46532] NR 3 TC 4 Z9 4 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1996 VL 28 IS 2 BP 791 EP 791 PG 1 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA UG383 UT WOS:A1996UG38300154 PM 8623401 ER PT J AU Dinsmore, JH Pakzaban, P Deacon, TW Burns, L Isacson, O AF Dinsmore, JH Pakzaban, P Deacon, TW Burns, L Isacson, O TI Survival of transplanted porcine neural cells treated with F(AB')(2) antibody fragments directed against donor MHC class-I in a rodent model SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 3rd International Congress for Xenotransplantation CY SEP 27-OCT 01, 1995 CL BOSTON, MA C1 MCLEAN HOSP,NEUROREGENERAT LAB,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,SERV NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. RP Dinsmore, JH (reprint author), DIACRIN,BLDG 96,13TH ST,BOSTON,MA 02129, USA. NR 5 TC 9 Z9 9 U1 0 U2 1 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1996 VL 28 IS 2 BP 817 EP 818 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA UG383 UT WOS:A1996UG38300168 PM 8623415 ER PT J AU Arita, S Saul, J Joh, S Kasraie, A Atiya, A Une, S Ohtsuka, S Mullen, Y AF Arita, S Saul, J Joh, S Kasraie, A Atiya, A Une, S Ohtsuka, S Mullen, Y TI Islet protective effect of pravastatin from nonspecific inflammation in mouse pancreatic islet isografts SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT Minneapolis Transplant Congress on New Immunosuppressive Drugs CY AUG 27-30, 1995 CL MINNEAPOLIS, MN SP Univ Minnesota, Dept Surg, Univ Minnesota, Continuing Med Educ, Univ Minnesota, Med Sch, Univ Minnesota, Continuing Educ Pharm, Univ Minnesota, CEE Univ Coll C1 W LOS ANGELES VET AFFAIRS MED CTR,HUMAN ISLET PROGRAM,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT SURG,VA UCLA HUMAN ISLET TRANSPLANT PROGRAM,LOS ANGELES,CA 90024. NR 4 TC 4 Z9 4 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1996 VL 28 IS 2 BP 924 EP 924 PG 1 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA UG383 UT WOS:A1996UG38300218 PM 8623465 ER PT J AU Miyamoto, M Kenmochi, T Nakagawa, Y Une, S Moldovan, S Atiya, A Benhamou, PY Brunicardi, FC Kawamura, M Kato, M Ohyanagi, H Mullen, Y AF Miyamoto, M Kenmochi, T Nakagawa, Y Une, S Moldovan, S Atiya, A Benhamou, PY Brunicardi, FC Kawamura, M Kato, M Ohyanagi, H Mullen, Y TI Establishment of an islet bank and its future perspectives SO TRANSPLANTATION PROCEEDINGS LA English DT Article ID PANCREAS C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT SURG,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP Miyamoto, M (reprint author), KINKI UNIV,SCH MED,DEPT SURG 2,377-2 OHNOHIGASHI,OSAKA 589,JAPAN. NR 8 TC 2 Z9 2 U1 1 U2 1 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1996 VL 28 IS 2 BP 1121 EP 1123 PG 3 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA UG383 UT WOS:A1996UG38300289 PM 8623246 ER PT J AU Orwoll, ES AF Orwoll, ES TI Androgens as anabolic agents for bone SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID IDIOPATHIC HYPOGONADOTROPIC HYPOGONADISM; NANDROLONE DECANOATE; MINERAL DENSITY; ELDERLY MEN; POSTMENOPAUSAL OSTEOPOROSIS; KLINEFELTERS-SYNDROME; SEX-DIFFERENCES; FEMALE RATS; WOMEN; TESTOSTERONE AB Androgens are classically considered anabolic agents, and in fact there is abundant evidence in many tissues that corroborates strong positive effects of androgens on proliferation and growth. In bone as well, there is clear evidence that androgen action is associated with an increase in skeletal mass, particularly during growth. Whether androgens can be considered anabolic in the skeleton later in life (when therapeutic increases in bone mass are of most clinical interest) is still a matter of some debate. RP Orwoll, ES (reprint author), OREGON HLTH SCI UNIV, PORTLAND VA MED CTR, BONE & MINERAL RES UNIT, PORTLAND, OR 97207 USA. OI Orwoll, Eric/0000-0002-8520-7355 NR 55 TC 33 Z9 33 U1 1 U2 2 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD APR PY 1996 VL 7 IS 3 BP 77 EP 84 DI 10.1016/1043-2760(96)00024-0 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UJ713 UT WOS:A1996UJ71300001 PM 18406730 ER PT J AU Narayan, P Trachtenberg, J Lepor, H Debruyne, FMJ Tewari, A Stone, N Das, S JimenezCruz, JF Shearer, R Klingbert, I Schellhammer, PF Costello, AJ ODonoghue, N Crawford, D Collste, L SchultzeSeemann Kirkemo, A Badelamant, R Wenderoth, UK Brawer, M Bouffioux, C McLeod, DG Flanigan, RC Gonick, P Breul, J Schick, E Kreigmair, M Kramer Frick, J Kaulen Bauer, H Jaske, G Heney, N AF Narayan, P Trachtenberg, J Lepor, H Debruyne, FMJ Tewari, A Stone, N Das, S JimenezCruz, JF Shearer, R Klingbert, I Schellhammer, PF Costello, AJ ODonoghue, N Crawford, D Collste, L SchultzeSeemann Kirkemo, A Badelamant, R Wenderoth, UK Brawer, M Bouffioux, C McLeod, DG Flanigan, RC Gonick, P Breul, J Schick, E Kreigmair, M Kramer Frick, J Kaulen Bauer, H Jaske, G Heney, N TI A dose-response study of the effect of flutamide on benign prostatic hyperplasia: Results of a multicenter study SO UROLOGY LA English DT Article ID NONSTEROIDAL ANTIANDROGEN; SCH 13521; HYPERTROPHY AB Objectives. The objective of this study was to evaluate efficacy, safety, and dose-response profiles of four dosing schemes of flutamide over 24 weeks. Methods. Patients were randomized to receive one of the following five treatment regimens for a period of 24 weeks: placebo capsule, flutamide capsules 125 mg twice daily, 250 mg once daily, 250 mg twice daily, and 250 mg three times daily. Patients were then evaluated at baseline (0 weeks) and at 4, 6, 12, 18, and 24 weeks after the start of treatment, and 8 weeks after the end of treatment (32 weeks). Evaluation of efficacy was performed by noting changes in urine flow rate, residual urine volume, symptom score, prostate volume, and prostate-specific antigen level. A total of 372 patients were enrolled into the study at 32 centers (14 centers in the United States and 18 international centers). Results. Baseline peak urinary flow rate and percent change from baseline in maximum flow rate showed a dose-related increase at 4 and 6 weeks; this increase was significant in the 250 mg three times daily group. At later time points, no significant differences between the flutamide and placebo groups were observed, largely because of the decreasing number of evaluable patients. At 4 and 6 weeks, 25% of patients in the 250 mg three times daily group had more than 3 cc/s increase in uroflow compared to about 10% of placebo patients (P < 0.05). All flutamide-treated groups had a significant decrease in prostate volume from baseline to the last treatment visit compared to placebo and this reduction was dose related (in comparison to placebo: P < 0.05 for 125 mg twice daily and P < 0.001 for all other treatment arms). Median decrease for the flutamide-treated groups ranged from 6% to 25% at 12 weeks and from 14% to 29% at 24 weeks. All treatment groups showed a subsequent increase in prostate volume after treatment was stopped. Furthermore, there was a significant reduction in residual urine volume at 24 weeks only in the 250 mg three times daily group. It increased following cessation of therapy. Urinary symptoms at 6, 12, 18, and 24 weeks did not show any significant difference between placebo and any flutamide dose group. The most common adverse events were nipple and breast tenderness (42% to 52%), diarrhea (29% to 34%), and gynecomastia (14% to 19%). Each of these adverse events had a significantly higher incidence in all flutamide dose groups compared with placebo, but none appeared to occur in a dose-related fashion. Sixteen percent of patients in the placebo group and 25% to 39% of patients in flutamide groups were discontinued due to diarrhea (12% to 17%) or nipple and breast tenderness (4% to 8%). A total of 1% to 3% of patients in various treatment arms discontinued due to deranged liver enzymes (1% for placebo); and 1% to 4% due to impotence (1% for placebo). Conclusions. Flutamide reduced the prostate volume in a dose-related fashion and resulted in an increase in peak flow rate at 4 weeks (3% for 250 mg three times daily, P value < 0.05), but the early positive effects did not maintain statistical significance due to an increasing number of dropouts due to adverse events. Effect on postvoid residual volume was observed only at the highest dose and at 24 weeks (median reduction, 25 mL, P < 0.05). Despite volume reduction and early improvement in peak flow rate, there were no significant differences in urinary symptoms among the placebo and flutamide groups. Higher incidences of diarrhea, breast tenderness, and gynecomastia, however, were the main limiting factors in this study and until these problems are overcome, the role of flutamide in the management of benign prostatic hyperplasia remains investigational. C1 UNIV FLORIDA,SCH MED,COLL MED,GAINESVILLE,FL 32610. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. DEPT VET AFFAIRS MED CTR,SAN FRANCISCO,CA. TORONTO GEN HOSP,TORONTO,ON,CANADA. MED COLL WISCONSIN,MILWAUKEE,WI 53226. ACAD HOSP RADBOND,NIJMEGEN,NETHERLANDS. MT SINAI HOSP,NEW YORK,NY 10029. KAISER PERMANENTE MED CORP HOSP,WALNUT CREEK,CA. HOSP LA FE,E-46009 VALENCIA,SPAIN. UNIV LONDON ST GEORGES HOSP,LONDON,ENGLAND. UROL CTR FLORIDA,OCALA,FL. SENTARA CANC INST,NORFOLK,VA. ST VINCENTS HOSP,MELBOURNE,VIC,AUSTRALIA. ST PETERS HOSP,LONDON WC2A 2EX,ENGLAND. UNIV COLORADO,DENVER,CO 80202. HUDDINGE HOSP,S-14186 HUDDINGE,SWEDEN. UNIV KLINIKUM FREIBURG,FREIBURG,GERMANY. HENRY FORD HOSP,DETROIT,MI 48202. OHIO STATE UNIV,COLUMBUS,OH 43210. UNIV KLIN,ULM,GERMANY. UNIV WASHINGTON,SEATTLE,WA 98195. CHU LIEGE,HOP BAVIERE,LIEGE,BELGIUM. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. UNIV MED SCH,MAYWOOD,IL. TECH UNIV MUNICH,UROL KLIN & POLIKLIN,W-8000 MUNICH,GERMANY. HOSP MAISONNEUVE ROSEMONT,MONTREAL,PQ,CANADA. UNIV FRANKFURT KLINIKUM,W-6000 FRANKFURT,GERMANY. ROLAND KLIN NIEDERSACHSENDAMM,BREMEN,GERMANY. RHEIN WESTFAL TH AACHEN,UROL CLIN,W-5100 AACHEN,GERMANY. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 20 TC 21 Z9 23 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD APR PY 1996 VL 47 IS 4 BP 497 EP 504 DI 10.1016/S0090-4295(99)80484-1 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA UM759 UT WOS:A1996UM75900011 PM 8638357 ER PT J AU Malkowicz, SB Vaughn, DJ AF Malkowicz, SB Vaughn, DJ TI Chemotherapy for invasive bladder cancer SO UROLOGY LA English DT Review ID TRANSITIONAL-CELL-CARCINOMA; M-VAC METHOTREXATE; ADVANCED UROTHELIAL CANCER; COLONY-STIMULATING FACTOR; GALLIUM NITRATE; ONCOLOGY-GROUP; PHASE-II; RIBONUCLEOTIDE REDUCTASE; CISPLATIN CHEMOTHERAPY; EUROPEAN ORGANIZATION C1 UNIV PENN, MED CTR, DEPT MED, DIV HEMATOL ONCOL, PHILADELPHIA, PA 19104 USA. VET AFFAIRS MED CTR, PHILADELPHIA, PA USA. RP Malkowicz, SB (reprint author), UNIV PENN, MED CTR,DEPT SURG,DIV UROL,1 RHOADS, 3400 SPRUCE ST, PHILADELPHIA, PA 19104 USA. NR 104 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0090-4295 J9 UROLOGY JI Urology PD APR PY 1996 VL 47 IS 4 BP 602 EP 614 PG 13 WC Urology & Nephrology SC Urology & Nephrology GA UM759 UT WOS:A1996UM75900035 PM 8638379 ER PT J AU Matsubara, O Yoshimura, N Doi, Y Tamura, A Mark, EJ AF Matsubara, O Yoshimura, N Doi, Y Tamura, A Mark, EJ TI Nasal biopsy in the early diagnosis of Wegener's (pathergic) granulomatosis - Significance of palisading granuloma and leukocytoclastic vasculitis SO VIRCHOWS ARCHIV-AN INTERNATIONAL JOURNAL OF PATHOLOGY LA English DT Article DE nasal mucosa; Wegener's granulomatosis; diagnosis; pathology; vasculitis ID SYSTEMIC VASCULITIS; AUTOANTIBODIES; ANTIBODIES; HEMORRHAGE AB The diagnostic value of the nasal biopsy in the early diagnosis of Wegener's granulomatosis and its value in prognosis were examined in 11 patients with a clinicopathological diagnosis of the disease. The vascular lesions found included microabscess in the vascular walls in 82%, leukocytoclastic capillaritis in 73%, fibrinoid necrosis of blood vessels in 45%, leukocytoclastic endovasculitis in 27%, and palisading granuloma in vascular wall in 9% of cases. The extravascular lesions included palisading granuloma in all cases, microabscess in 91%, and diffuse granulomatous tissues in 82%. Palisading microgranuloma (82%) was more frequent than palisading macrogranuloma (45%). After therapy, complete remission occurred in 8 patients, but 3 patients died of sepsis, diffuse pulmonary haemorrhage, and cerebral haemorrhage. Comparison of the frequency of each finding in the nasal biopsy specimens between patients who achieved remission and those who died showed that leukocytoclastic vasculitis was found more commonly in fatal cases, and leukocytoclastic endovasculitis was observed only in fatal cases. Palisading granuloma as a vascular or extravascular lesion is the primary and most important finding in a histopathological diagnosis of Wegener's granulomatosis, microabscess in vascular walls is a secondary but the next most important finding, and leukocytoclastic vasculitis heralds dissemination of the disease and poor prognosis. It requires aggressive therapy. C1 TOKYO MED & DENT UNIV,FAC MED,DEPT PATHOL,TOKYO 113,JAPAN. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP Matsubara, O (reprint author), NATL DEF MED COLL,DEPT PATHOL,3-2 NAMIKI,TOKOROZAWA,SAITAMA 359,JAPAN. NR 17 TC 17 Z9 17 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0945-6317 J9 VIRCHOWS ARCH JI Virchows Arch. Int. J. Pathol. PD APR PY 1996 VL 428 IS 1 BP 13 EP 19 PG 7 WC Pathology SC Pathology GA UN142 UT WOS:A1996UN14200003 PM 8646364 ER PT J AU Wilk, T Pfeiffer, T Bukovsky, A Moldenhauer, G Bosch, V AF Wilk, T Pfeiffer, T Bukovsky, A Moldenhauer, G Bosch, V TI Glycoprotein incorporation and HIV-1 infectivity despite exchange of the gp160 membrane-spanning domain SO VIROLOGY LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; ENV GENE-PRODUCT; ENVELOPE GLYCOPROTEINS; OVERLAP EXTENSION; AIDS VIRUS; MUTANTS; SITE; IDENTIFICATION; MUTAGENESIS; RETROVIRUS AB We have examined the role of the membrane-anchoring domain of the HIV-1 glycoproteins in viral glycoprotein function, glycoprotein incorporation, and viral infectivity. For this purpose, we initially exchanged the entire membrane-spanning region with that from a cellular glycoprotein (CD22). Subsequently, the strictly conserved arginine in the central position of the transmembranal alpha-helix was replaced by a neutral residue (R(696) --> I-696). We have further examined the requirements within the cytoplasmic C-terminus for glycoprotein incorporation and replaced this region of gp160 with the long cytoplasmic C-terminus (118 amino acids) from CD22. Our results show that the specific amino acid sequence of the membrane-spanning region of gp160 is not necessary for viral infectivity, thus making it unlikely that this region is specifically involved in membrane fusion, in glycoprotein incorporation, or in infectivity of the cell lines tested. In contrast, recombinant gp160 with the CD22 C-terminal region, although present at the cell surface and membrane fusion-competent, was excluded from incorporation into particles. This could indicate that steric exclusion, and no pseudotyping, occurs when the heterologous, cytoplasmic C-terminal region is too long and not fitting. (C) 1996 Academic Press, Inc. C1 DEUTSCH KREBSFORSCHUNGSZENTRUM, FORSCH SCHWERPUNKT ANGEW TUMORVIROL, D-69120 HEIDELBERG, GERMANY. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV HUMAN RETROVIROL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. NR 26 TC 41 Z9 41 U1 1 U2 6 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0042-6822 J9 VIROLOGY JI Virology PD APR 1 PY 1996 VL 218 IS 1 BP 269 EP 274 DI 10.1006/viro.1996.0190 PG 6 WC Virology SC Virology GA UD495 UT WOS:A1996UD49500031 PM 8615034 ER PT J AU Wharton, RH Wang, T GraemeCooke, F Briggs, S AF Wharton, RH Wang, T GraemeCooke, F Briggs, S TI Acute gastric dilation and gastric necrosis and death in individuals with Prader-Willi syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD MAR 29 PY 1996 VL 62 IS 3 BP 12 EP 12 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA UC681 UT WOS:A1996UC68100013 ER PT J AU Prence, EM Gleason, J Natowicz, MR AF Prence, EM Gleason, J Natowicz, MR TI Characterization of clinical assays for leukocyte and fibroblast alpha-N-acetylgalactosaminidase activities for the diagnosis of alpha-N-acetylgalactosaminidase deficiency SO CLINICA CHIMICA ACTA LA English DT Article DE alpha-N-acetylgalactosaminidase; lysosomal storage disease; Schindler disease ID ANGIOKERATOMA-CORPORIS-DIFFUSUM; DISEASE C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP Prence, EM (reprint author), EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV MED GENET,200 TRAPELO RD,WALTHAM,MA 02254, USA. NR 15 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0009-8981 J9 CLIN CHIM ACTA JI Clin. Chim. Acta PD MAR 29 PY 1996 VL 247 IS 1-2 BP 167 EP 173 DI 10.1016/0009-8981(95)06240-8 PG 7 WC Medical Laboratory Technology SC Medical Laboratory Technology GA UC515 UT WOS:A1996UC51500014 PM 8920235 ER PT J AU Bang, OS Ruscetti, FW Lee, MH Kim, SJ BirchenallRoberts, MC AF Bang, OS Ruscetti, FW Lee, MH Kim, SJ BirchenallRoberts, MC TI Transforming growth factor-beta 1 modulates p107 function in myeloid cells - Correlation with cell cycle progression SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RETINOBLASTOMA GENE-PRODUCT; TRANSCRIPTION FACTOR E2F; FACTOR-BETA; TGF-BETA; NEGATIVE REGULATION; CATALYTIC SUBUNIT; DEPENDENT KINASE; MAMMALIAN-CELLS; PROTEIN-KINASE; DNA-SYNTHESIS AB Transforming growth factor-beta 1 (TGF-beta 1) is a potent inhibitor of hematopoietic cell growth. Here we report that TGF-beta 1 signals inhibition of IL-3-dependent 32D-123 murine myeloid cell growth by modulating the activities of cyclin E and cyclin-dependent kinase 2 (cdk2) proteins and their complex formation in the G(1) phase of the cell cycle. Whereas the cyclin E protein was hyperphosphorylated in TGF-beta 1-treated cells, TGF-beta 1 decreased both the phosphorylation of cdk2 and the kinase activity of the cyclin E-cdk2 complex. Decreased cyclin E-cdk2 kinase activity correlated with decreased phosphorylation of the retinoblastoma-related protein p107. In support of these observations, transient overexpression of p107 inhibited the proliferation of the myeloid cells, and expression of antisense oligo deoxynucleotides to p107 mRNA blocked TGF-beta 1 inhibition of myeloid cell growth. Furthermore, as reported previously, in 32D-123 TGF-beta 1-treated cells, c-Myc protein expression was decreased. TGF-beta 1 increased the binding of p107 to the transcription factor E2F, leading to decreased c-Myc protein levels, p107 inhibited E2F transactivation activity and was also found to bind the c-Myc protein, suggesting p107 negative regulation of c-Myc protein function. These studies demonstrate the modulation of p107 function by TGF-beta 1 and suggest a novel mechanism by which TGF-beta 1 blocks cell cycle progression in myeloid cells. C1 NCI,CHEMOPREVENT LAB,NIH,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP CANC CTR,MOLEC ONCOL LAB,BOSTON,MA 02129. NCI,BIOL CARCINOGENESIS & DEV PROGRAM,SAIC FREDERICK,NIH,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NCI,LAB LEUKOCYTE BIOL,DIV BASIC SCI,NIH,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NCI,DIV CANC TREATMENT,NIH,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. NR 73 TC 9 Z9 10 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 29 PY 1996 VL 271 IS 13 BP 7811 EP 7819 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UC774 UT WOS:A1996UC77400093 PM 8631825 ER PT J AU Mecocci, P Cherubini, A Beal, MF Cecchetti, R Chionne, F Polidori, MC Romano, G Senin, U AF Mecocci, P Cherubini, A Beal, MF Cecchetti, R Chionne, F Polidori, MC Romano, G Senin, U TI Altered mitochondrial membrane fluidity in AD brain SO NEUROSCIENCE LETTERS LA English DT Article DE mitochondria; membrane fluidity; oxidative stress; aging; Alzheimer's disease ID LIPID-PEROXIDATION; ALZHEIMERS-DISEASE; INCREASES; REGIONS AB Oxidative damage on biological membranes has been proposed as a cause of the alterations observed in aging brain and, more severely, in Alzheimer's disease (AD). In this study we evaluated membrane fluidity of mitochondria extracted from different areas of normal and AD brains by means of fluorescence polarization technique. AD mitochondria showed a significant reduction of membrane fluidity compared to controls except in cerebellum. This might be caused by a greater lipid peroxidation of biological membranes, as suggested by in vitro experiments we performed to this purpose. From these results the possible role of oxidative stress in AD pathogenesis is supported. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,NEUROCHEM LAB,BOSTON,MA. MONTELUCE POLICLIN,DEPT MED PHYS,PERUGIA,ITALY. RP Mecocci, P (reprint author), UNIV PERUGIA,DEPT CLIN MED PATHOL & PHARMACOL,VIA EUGUBINA 42,I-06122 PERUGIA,ITALY. OI Cherubini, Antonio/0000-0003-0261-9897 NR 24 TC 38 Z9 45 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD MAR 29 PY 1996 VL 207 IS 2 BP 129 EP 132 DI 10.1016/0304-3940(96)12509-X PG 4 WC Neurosciences SC Neurosciences & Neurology GA UH284 UT WOS:A1996UH28400015 PM 8731438 ER PT J AU Testa, MA Simonson, DC AF Testa, MA Simonson, DC TI Current concepts - Assessment of quality-of-life outcomes SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID IMPACT MEASUREMENT SCALES; HEALTH-STATUS; CLINICAL-TRIALS; ANTIHYPERTENSIVE THERAPY; STATUS QUESTIONNAIRE; FUNCTIONAL STATUS; ARTHRITIS; DISEASE; CARE C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DEPT MED,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. RP Testa, MA (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,677 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 46 TC 1128 Z9 1187 U1 3 U2 26 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 28 PY 1996 VL 334 IS 13 BP 835 EP 840 DI 10.1056/NEJM199603283341306 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA UB950 UT WOS:A1996UB95000006 PM 8596551 ER PT J AU Back, AL Wallace, JI Starks, HE Pearlman, RA AF Back, AL Wallace, JI Starks, HE Pearlman, RA TI Physician-assisted suicide and euthanasia in Washington State - Patient requests and physician responses SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID DEATH; DECISIONS; LIFE AB Objectives.-To estimate how often physicians receive requests for physician-assisted suicide and euthanasia and to describe a case series of patient requests for physician-assisted suicide and euthanasia, including physician responses to these requests. Design.-A mailed, anonymous two-part questionnaire. Participants.-A total of 828 physicians returned questionnaires sent to 1453 potential respondents, for a response rate of 57%. Questionnaires were mailed to a random sample (25%) of primary care physicians and all physicians in selected medical subspecialties in Washington State. Main Outcome Measures.-The frequency of explicit patient requests for physician-assisted suicide and euthanasia reported by physicians and individual case descriptions of patient characteristics, physician perceptions of patient concerns, and physician responses to patient requests. Results.-In the past year, 12% of responding physicians received one or more explicit requests for physician-assisted suicide, and 4% received one or more requests for euthanasia. These physicians provided 207 case descriptions. The diagnoses most often associated with requests were cancer, neurological disease, and the acquired immunodeficiency syndrome (AIDS). The patient concerns most often perceived by physicians were worries about loss of control, being a burden, being dependent on others for personal care, and loss of dignity, Physicians provided assistance more often to patients with physical symptoms. Physicians infrequently sought advice from colleagues, Of 156 patients who requested physician-assisted suicide, 38 (24%) received prescriptions, and 21 of these died as a result. Of 58 patients who requested euthanasia, 14 (24%) received parenteral medication and died. Conclusions.-Patient requests for physician-assisted suicide and euthanasia are not rare, As perceived by physicians, the most common patient concerns at the time these requests are made are nonphysical, Physicians occasionally provide these practices, even though they are currently illegal in Washington State. Physicians do not consult colleagues often about these requests. These findings raise the question of how to ensure quality in the evaluation of patient requests for physician-assisted death. C1 VET AFFAIRS PUGET SOUND HLTH CARE SYST,CTR GERIATR RES EDUC & CLIN,SEATTLE,WA 98108. UNIV WASHINGTON,SCH MED,DEPT MED,SEATTLE,WA 98195. UNIV WASHINGTON,SCH MED,DEPT MED HIST & ETH,SEATTLE,WA 98195. UNIV WASHINGTON,SCH PUBL HLTH,DEPT HLTH SERV,SEATTLE,WA 98195. RP Back, AL (reprint author), VET AFFAIRS PUGET SOUND HLTH CARE SYST,MED SERV,1660 S COLUMBIAN WAY,SEATTLE,WA 98108, USA. FU NIA NIH HHS [AG00615-02] NR 37 TC 249 Z9 249 U1 4 U2 26 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 27 PY 1996 VL 275 IS 12 BP 919 EP 925 DI 10.1001/jama.275.12.919 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA UA563 UT WOS:A1996UA56300031 PM 8598619 ER PT J AU Sager, MA Franke, T Inouye, SK Landefeld, CS Morgan, TM Rudberg, MA Siebens, H Winograd, CH AF Sager, MA Franke, T Inouye, SK Landefeld, CS Morgan, TM Rudberg, MA Siebens, H Winograd, CH TI Functional outcomes of acute medical illness and hospitalization in older persons SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID PROSPECTIVE PAYMENT SYSTEM; CARE; IMPLEMENTATION; COMPLICATIONS; QUALITY; SERVICE; TRIAL AB Background: Short-stay hospitalization in older patients is frequently associated with a loss of function, which can lead to a need for postdischarge assistance and longer-term institutionalization. Because little is known about this adverse outcome of hospitalization, this study was conducted to (1) determine the discharge and 3-month postdischarge functional outcomes for a large cohort of older persons hospitalized for medical illness, (2) determine the extent to which patients were able to recover to preadmission levels of functioning after hospital discharge, and (3) identify the patient factors associated with an increased risk of developing disability associated with acute illness and hospitalization. Methods: A total of 1279 community-dwelling patients, aged 70 rears and older, hospitalized for acute medical illness were enrolled in this multicenter, prospective cohort study. Functional measurements obtained at discharge (Activities of Daily Living) and at 3 months after discharge (Activities of Daily Living and Instrumental Activities of Daily Living) were compared with a preadmission baseline level of functioning to document loss and recovery of functioning. Results: At discharge, 59% of the study population reported no-change, 10% improved, and 31% declined in Activities of Daily Living when compared with the preadmission baseline. At the 3-month follow-up, 51% of the original study population, for whom postdischarge data were available (n=1206),were found to have died (11%) or to report new Activities of Daily Living and/or Instrumental Activities of Daily Living disabilities (40%) when compared with the preadmission baseline. Among survivors, 19% reported a new Activities of Daily Living and 40% reported a new Instrumental Activities of Daily Living disability at follow-up. The 3-month outcomes were the result of the loss of function during the index hospitalization, the failure of many patients to recover after discharge, and the development of new postdischarge disabilities. Patients at greatest risk of adverse functional outcomes at follow-up were older, had preadmission Instrumental Activities of Daily Living disabilities and lower mental status scores on admission, and had been rehospitalized. Conclusions: This study documents a high incidence of functional decline after hospitalization for acute medical illness. Although there are several potential explanations for these findings, this study suggests a need to reexamine current inpatient and postdischarge practices that might influence the functioning of older patients. C1 UNIV WISCONSIN,DEPT MED & PREVENT MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV CALIF LOS ANGELES,DEPT SOCIAL WELFARE,LOS ANGELES,CA. YALE UNIV,SCH MED,DEPT INTERNAL MED,NEW HAVEN,CT 06510. CASE WESTERN RESERVE UNIV,SCH MED,CLEVELAND,OH. VET AFFAIRS MED CTR,CLEVELAND,OH. UNIV HOSP CLEVELAND,CLEVELAND,OH 44106. BOWMAN GRAY SCH MED,DEPT PUBL HLTH SCI,WINSTON SALEM,NC. UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. CEDARS SINAI MED CTR,DEPT PHYS MED & PHYS REHABIL,LOS ANGELES,CA. STANFORD UNIV,SCH MED,DEPT MED,PALO ALTO,CA 94304. VET AFFAIRS MED CTR,PALO ALTO,CA 94304. NR 36 TC 279 Z9 284 U1 0 U2 12 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD MAR 25 PY 1996 VL 156 IS 6 BP 645 EP 652 DI 10.1001/archinte.156.6.645 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA UB001 UT WOS:A1996UB00100006 PM 8629876 ER PT J AU Cohen, LG Chesley, S Eugenio, L Flood, JG Fisch, J Goff, DC AF Cohen, LG Chesley, S Eugenio, L Flood, JG Fisch, J Goff, DC TI Erythromycin-induced clozapine toxic reaction SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID THEOPHYLLINE AB Clozapine, used in the treatment of patients with schizophrenia resistant to other neuroleptic medication, is metabolized by the hepatic microsomal system to demethylclozapine and clozapine-N-oxide. Changes in clozapine serum concentrations have been documented after initiation of therapy with medications known to induce or inhibit liver microsomal enzymes. These interactions are of clinical importance when diminished efficacy or increased toxic effects of clozapine therapy occur. A 34-year-old schizophrenic man had increased clozapine serum concentrations, leukocytosis, and adverse effects as a result of concomitant erythromycin therapy given for a suspected lower respiratory tract infection. Symptoms included somnolence, difficulty in coordination and ambulation, slurred speech, disorientation, and incontinence. The symptoms resolved after treatment with clozapine and erythromycin were discontinued, and treatment with clozapine was gradually resumed. C1 NORTHEASTERN UNIV,BOUVE COLL PHARM,DEPT PHARM PRACTICE,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT CLIN CHEM,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. MASSACHUSETTS COLL PHARM & ALLIED HLTH SCI,DIV PHARM PRACTICE,BURLINGTON,MA. LAHEY CLIN FDN,DEPT PHARM,BURLINGTON,MA. RP Cohen, LG (reprint author), MASSACHUSETTS GEN HOSP,DEPT PHARM,VBK BA 020,BOSTON,MA 02114, USA. NR 15 TC 46 Z9 46 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD MAR 25 PY 1996 VL 156 IS 6 BP 675 EP 677 DI 10.1001/archinte.156.6.675 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA UB001 UT WOS:A1996UB00100011 PM 8629881 ER PT J AU Kirschner, PB Jenkins, BG Schulz, JB Finkelstein, SP Matthews, RT Rosen, BR Beal, MF AF Kirschner, PB Jenkins, BG Schulz, JB Finkelstein, SP Matthews, RT Rosen, BR Beal, MF TI NGF, BDNF and NT-5, but not NT-3 protect against MPP(+) toxicity and oxidative stress in neonatal animals SO BRAIN RESEARCH LA English DT Article DE neurotrophin; nerve growth factor; 1-methyl-4-phenylpyridinium; mitochondrion; Parkinson's disease ID NERVE GROWTH-FACTOR; HYDROXYL RADICAL GENERATION; HIPPOCAMPAL-NEURONS; CALCIUM HOMEOSTASIS; NEUROTROPHIC FACTOR; BRAIN; ACID; SURVIVAL; SYSTEM; INJURY AB A growing body of evidence suggests that neurotrophic factors can protect neurons against neuronal death. In the present study we examined whether systemic administration of members of the neurotrophin family, nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3) and neurotrophin 5 (NT-5) and basic fibroblast growth factor (bFGF) could protect against 1-methyl-4-phenylpyridinium (MPP(+)) induced striatal damage in neonatal rats. Systemic administration of NGF, BDNF and NT-5 produced significant neuroprotective effects, whereas NT-3 was ineffective. Systemic administration of bFGF had significant neuroprotective effects as assessed by T-2-weighted magnetic resonance imaging and measurements of n-acetylaspartate and lactate using chemical shift magnetic resonance imaging. Systemic administration of NGF, BDNF and bFGF, but not NT-3 attenuated MPP(+) induced increases in hydroxyl radical generation as assessed by the conversion of salicylate to 2,3- or 2,5-dihydroxybenzoic acid (DHBA). These results show that systemic administration of several neurotrophins and bFGF can attenuate neuronal damage induced by chemical hypoxia in vivo by a mechanism which may involve attenuation of oxidative stress. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,NEUROCHEM LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROL SERV,MGH NMR CTR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,CNS GROWTH FACTOR LAB,BOSTON,MA 02114. RI Schulz, Jorg/D-9786-2012 OI Schulz, Jorg/0000-0002-8903-0593 FU NINDS NIH HHS [NS10878, NS31579]; PHS HHS [16367] NR 47 TC 68 Z9 71 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 25 PY 1996 VL 713 IS 1-2 BP 178 EP 185 DI 10.1016/0006-8993(95)01513-2 PG 8 WC Neurosciences SC Neurosciences & Neurology GA UE900 UT WOS:A1996UE90000021 PM 8724989 ER PT J AU Gill, DS Wong, YW ParhamiSeren, B Short, MK Margolies, MN AF Gill, DS Wong, YW ParhamiSeren, B Short, MK Margolies, MN TI Structure-function studies of a phage-displayed anti-arsonate antibody SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,LAB ANTIBODY ENGN,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 24 PY 1996 VL 211 BP 125 EP BIOT PN 1 PG 1 WC Chemistry, Multidisciplinary SC Chemistry GA UA482 UT WOS:A1996UA48200580 ER PT J AU LeDoux, JM Morgan, JR Yarmush, ML AF LeDoux, JM Morgan, JR Yarmush, ML TI Proteoglycans secreted by packaging cell Lines inhibit retroviral-mediated gene transfer. SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD MAR 24 PY 1996 VL 211 BP 224 EP BIOT PN 1 PG 1 WC Chemistry, Multidisciplinary SC Chemistry GA UA482 UT WOS:A1996UA48200679 ER PT J AU Durante, W Kroll, MH Orloff, GJ Cunningham, JM Scottburden, T Vanhoutte, PM Schafer, AI AF Durante, W Kroll, MH Orloff, GJ Cunningham, JM Scottburden, T Vanhoutte, PM Schafer, AI TI Regulation of interleukin-1 beta-stimulated inducible nitric oxide synthase expression in cultured vascular smooth muscle cells by hemostatic proteins SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE smooth muscle; nitric oxide; hemostasis ID L-ARGININE; MOUSE MACROPHAGES; INDUCTION; ENDOTOXIN; CYTOKINES; CLONING; RESPONSIVENESS; ENDOTHELIUM; HEPATOCYTES; OXIDATION AB Experiments were performed to examine the mechanism by which specific hemostatic proteins regulate the release of nitric oxide (NO) from interleukin-1 beta (IL-1 beta) stimulated cultured rat aortic smooth muscle cells. Treatment of smooth muscle cells with IL-beta stimulated inducible nitric oxide synthase (iNOS) mRNA expression, which preceded the release of NO (as measured by the accumulation of nitrite in the culture media). The cytokine-stimuiated production of nitrite was blocked by the protein synthesis inhibitor cycloheximide, the transcriptional inhibitor actinomycin D, and the competitive inhibitor of NOS nitro-L-arginine. However, only actinomycin D inhibited IL-1 beta-stimulated iNOS mRNA expression. Treatment of smooth muscle cells with IL-1 beta in the presence of platelet derived growth factor or thrombin resulted in the inhibition of cytokine-stimulated expression of iNOS mRNA and NO release. The inhibitory effect of thrombin was reversed by hirudin and was mimicked by a 14 amino acid thrombin receptor activating peptide. In contrast, the concomitant exposure of smooth muscle cells to IL-1 beta and plasmin resulted in the potentiation of both IL-1 beta-stimulated iNOS expression and NO generation. Finally, treatment of smooth muscle cells with IL-1 beta in the presence of the hemostatic proteins did not affect the half-life of iNOS mRNA. These results demonstrate that specific protein components of the hemostatic system regulate IL-1 beta-stimulated iNOS mRNA expression in vascular smooth muscle cells. The capacity of hemostatic proteins to modulate the induction of vascular iNOS activity may play an important role in governing the release of NO and regulating thrombogenesis in vivo. C1 BAYLOR COLL MED,DEPT MED & PHARMACOL,HOUSTON,TX 77030. BAYLOR COLL MED,CTR EXPTL THERAPEUT,HOUSTON,TX 77030. BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. RP Durante, W (reprint author), HOUSTON VA MED CTR,MED SERV,BLDG 109,ROOM 116,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. RI Vanhoutte, Paul/B-4533-2009 FU NHLBI NIH HHS [HL-31183, HL-36045, HL-02311] NR 35 TC 15 Z9 15 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAR 22 PY 1996 VL 51 IS 6 BP 847 EP 853 DI 10.1016/0006-2952(95)02409-3 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TZ107 UT WOS:A1996TZ10700016 PM 8602881 ER PT J AU Qu, DQ Ludwig, DS Gammeltoft, S Piper, M Pelleymounter, MA Cullen, MJ Mathes, WF Przypek, J Kanarek, R MaratosFlier, E AF Qu, DQ Ludwig, DS Gammeltoft, S Piper, M Pelleymounter, MA Cullen, MJ Mathes, WF Przypek, J Kanarek, R MaratosFlier, E TI A role for melanin-concentrating hormone in the central regulation of feeding behaviour SO NATURE LA English DT Article ID MESSENGER-RIBONUCLEIC-ACID; RAT-BRAIN; PUTATIVE NEUROPEPTIDES; HYPOTHALAMUS; PEPTIDE; GENE; LOCALIZATION; STIMULATION; SYSTEM; RNA AB THE hypothalamus plays a central role in the integrated regulation of energy homeostasis and body weight, and a number of hypothalamic neuropeptides, such as neuropeptide Y (ref. 1), galanin(2), CRH (ref. 3), and GLP-1 (ref. 4), have been implicated in the mediation of these effects. To discover new hypothalamic peptides involved in the regulation of body weight, we used differential display polymerase chain reaction(5) to identify messenger RNAs that are differentially expressed in the hypothalamus of ob/+ compared with ob/ob C57Bl/6J mice. We show here that one mRNA that is overexpressed in the hypothalamus of ob/ob mice encodes the neuropeptide melanin-concentrating hormone (MCH). Fasting further increased expression of MCH mRNA in both normal and obese animals. Neurons containing MCH are located in the zona incerta and in the lateral hypothalamus. These areas are involved in regulation of ingestive behaviour, but the role of MCH in mammalian physiology is unknown. To determine whether MCH is involved in the regulation of feeding, we injected MCH into the lateral ventricles of rats and found that their food consumption increased. These findings suggest that MCH participates in the hypothalamic regulation of body weight. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,ELLIOT P JOSLIN RES LAB,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02215. BETH ISRAEL HOSP,DEPT MED,DIV ENDOCRINOL,BOSTON,MA 02215. AMGEN INC,DEPT NEUROBIOL,THOUSAND OAKS,CA 91320. TUFTS UNIV,DEPT PSYCHOL,MEDFORD,MA 02155. NR 30 TC 960 Z9 976 U1 1 U2 35 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD MAR 21 PY 1996 VL 380 IS 6571 BP 243 EP 247 DI 10.1038/380243a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UB117 UT WOS:A1996UB11700050 PM 8637571 ER PT J AU Mankin, HJ Wu, HC Marianacci, EB Cohen, ME Mark, EJ Colvin, RB Heller, HM AF Mankin, HJ Wu, HC Marianacci, EB Cohen, ME Mark, EJ Colvin, RB Heller, HM TI A 21-year-old African woman with thoracolumbar pain and fever - Vertebral tuberculosis. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID NEEDLE ASPIRATION BIOPSY; FEMALE CIRCUMCISION; SPINAL TUBERCULOSIS; BONE; COMPLICATIONS; LYMPHOMA; SOMALIA C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. RP Mankin, HJ (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED SERV,BOSTON,MA 02114, USA. NR 33 TC 1 Z9 1 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 21 PY 1996 VL 334 IS 12 BP 784 EP 789 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA TZ979 UT WOS:A1996TZ97900008 ER PT J AU Geng, Y Eaton, EN Picon, M Roberts, JM Lundberg, AS Gifford, A Sardet, C Weinberg, RA AF Geng, Y Eaton, EN Picon, M Roberts, JM Lundberg, AS Gifford, A Sardet, C Weinberg, RA TI Regulation of cyclin E transcription by E2Fs and retinoblastoma protein SO ONCOGENE LA English DT Article DE cell cycle; cyclin E transcription; E2F; retinoblastoma protein ID CELL-CYCLE; DEPENDENT KINASES; BINDING PROTEIN; CDC2 GENE; EXPRESSION; REPRESSION; CLONING; PHOSPHORYLATION; TRANSACTIVATION; ASSOCIATION AB Cyclin E is critical for the advance of cells through the G1 phase of their growth cycle. Transcription of the cyclin E gene is known to be cell cycle-dependent. We have shown previously that mRNA levels of cyclin E are regulated positively by mitogens and negatively by TGF-beta. Much circumstantial evidence implicates both E2F transcription factors and the retinoblastoma protein (pRB) in the control of cyclin E expression. However, the molecular basis of this control has remained unclear. We report here the cloning of the cyclin E promoter and the identification of several putative E2F binding sites within the promoter sequence. We have found that cell cycle regulation of cyclin E transcription is mediated by E2F binding sites present in the promoter. The activity of this promoter can be regulated negatively by pRB. Our results suggest the operation of a positive-feedback loop in late G1 that functions to ensure continued cyclin E expression and pRB inactivation. C1 WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. FRED HUTCHINSON CANC RES CTR,DEPT BASIC SCI,SEATTLE,WA 98104. DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [R35-CA39826] NR 50 TC 329 Z9 341 U1 1 U2 13 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR 21 PY 1996 VL 12 IS 6 BP 1173 EP 1180 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA UC067 UT WOS:A1996UC06700001 PM 8649818 ER PT J AU Enders, GH Koh, J Missero, C Rustgi, AK Harlow, E AF Enders, GH Koh, J Missero, C Rustgi, AK Harlow, E TI p16 inhibition of transformed and primary squamous epithelial cells SO ONCOGENE LA English DT Article DE p16; esophageal squamous cell carcinoma; retinoblastoma protein; squamous epithelial ID RETINOBLASTOMA PROTEIN; CYCLE CONTROL; PHOSPHORYLATION; DIFFERENTIATION; MOUSE; GENE AB We and others have recently shown that p16 can potently and specifically inhibit progression through the G1 phase of the replicative cycle in cells that express the retinoblastoma protein (pRB). However, none of these studies examined cell types in which p16 has been firmly implicated in tumorigenesis. We predicted that such cells would show sensitivity to p16 inhibition, perhaps conferred by proteins in addition to or other than pRB. Intragenic, inactivating mutations of p16 have been found at significant frequency in primary tumors derived from squamous epithelial cells of the esophagus (ESCC). We therefore examined p16 function in ESCC lines and in primary squamous epithelial cells cultured from mouse skin. We find that seven of eight ESCC lines tested are inhibited by p16 and fail to express the protein endogenously. The lone p16-resistant line expresses endogenous p16 but lacks functional pRB. Primary squamous epithelial cells are also inhibited by p16. These data suggest that squamous epithelial cells are generally sensitive to inhibition by a regulatory pathway that involves p16 and pRB, and that, by the time of establishment in culture, there is nearly universal inactivation of this pathway in ESCCs. C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. RP Enders, GH (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129, USA. NR 36 TC 41 Z9 41 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAR 21 PY 1996 VL 12 IS 6 BP 1239 EP 1245 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA UC067 UT WOS:A1996UC06700009 PM 8649826 ER PT J AU Weiss, R Paoletti, E Jarrett, O Stott, J Esparza, J Montagnier, L Essex, M Kurth, R Bangham, C deThe, G Bruck, C Sattentau, Q Ruprecht, R Girard, M McConnell, I Pancino, G Hu, SL AF Weiss, R Paoletti, E Jarrett, O Stott, J Esparza, J Montagnier, L Essex, M Kurth, R Bangham, C deThe, G Bruck, C Sattentau, Q Ruprecht, R Girard, M McConnell, I Pancino, G Hu, SL TI Roundtable: Can experience with veterinary retroviral vaccines be applied to the human situation? SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Discussion C1 INST PASTEUR, UNITE EPIDEMIOL VIRUS ONCOGENES, F-75724 PARIS, FRANCE. ROYAL CANC HOSP, INST CANC RES, LONDON, ENGLAND. VIROGENET CORP, TROY, NY 12180 USA. UNIV GLASGOW, DEPT VET PATHOL, GLASGOW, LANARK, SCOTLAND. NATL INST BIOL STAND & CONTROLS, S MIMMS, HERTS, ENGLAND. WHO, CH-1211 GENEVA, SWITZERLAND. INST PASTEUR, UNITE ONCOL VIRALE, F-75724 PARIS, FRANCE. HARVARD UNIV, AIDS INST, BOSTON, MA 02115 USA. PAUL EHRLICH INST, W-6070 LANGEN, GERMANY. JOHN RADCLIFFE HOSP, DEPT MICROBIOL, OXFORD OX3 9DU, OXON, ENGLAND. SMITHKLINE BEECHAM BIOL, RIXENSART, BELGIUM. CTR IMMUNOL MARSEILLE LUMINY, MARSEILLE, FRANCE. HARVARD UNIV, SCH MED, LAB VIRAL PATHOGENESIS, BOSTON, MA USA. DANA FARBER CANC INST, BOSTON, MA 02115 USA. INST PASTEUR, UNITE VIROL MOL, PARIS, FRANCE. UNIV CAMBRIDGE, CTR VET SCI, CAMBRIDGE, ENGLAND. INST COCHIN GENET MOLEC, F-75014 PARIS, FRANCE. BRISTOL MYERS SQUIBB PHARMACEUT RES INST, SEATTLE, WA USA. RI Pancino, Gianfranco/A-5519-2010 NR 0 TC 3 Z9 3 U1 0 U2 3 PU MARY ANN LIEBERT, INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 0889-2229 EI 1931-8405 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAR 20 PY 1996 VL 12 IS 5 BP 365 EP 373 PG 9 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA UA592 UT WOS:A1996UA59200004 ER PT J AU Ruprecht, RM Hu, YW Liska, V Rasmussen, R Sharma, P AF Ruprecht, RM Hu, YW Liska, V Rasmussen, R Sharma, P TI Correlates of immune protection after vaccination with attenuated live murine leukemia virus SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Workshop on Comparative Approach to Retroviral Vaccines CY JUN 23-24, 1995 CL LES PENSIERES CONF CTR, VEYRIER DU LAC, FRANCE SP Fdn Marcel Merieux HO LES PENSIERES CONF CTR ID INDUCED ERYTHROLEUKEMIA; RETROVIRUS C1 HARVARD UNIV,SCH MED,LAB VIRAL PATHOGENESIS,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02115. RP Ruprecht, RM (reprint author), DANA FARBER CANC INST,LAB VIRAL PATHOGENESIS,44 BINNEY ST,BOSTON,MA 02115, USA. NR 14 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAR 20 PY 1996 VL 12 IS 5 BP 375 EP 377 DI 10.1089/aid.1996.12.375 PG 3 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA UA592 UT WOS:A1996UA59200005 PM 8882313 ER PT J AU Ruprecht, RM Baba, TW Liska, V Bronson, R Penninck, D Greene, MF AF Ruprecht, RM Baba, TW Liska, V Bronson, R Penninck, D Greene, MF TI ''Attenuated'' simian immunodeficiency virus in macaque neonates SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article; Proceedings Paper CT Workshop on Comparative Approach to Retroviral Vaccines CY JUN 23-24, 1995 CL LES PENSIERES CONF CTR, VEYRIER DU LAC, FRANCE SP Fdn Marcel Merieux HO LES PENSIERES CONF CTR C1 HARVARD UNIV,SCH MED,LAB VIRAL PATHOGENESIS,BOSTON,MA 02115. TUFTS UNIV,SCH MED,BOSTON,MA 02111. TUFTS UNIV,SCH VET MED,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Ruprecht, RM (reprint author), DANA FARBER CANC INST,LAB VIRAL PATHOGENESIS,44 BINNEY ST,BOSTON,MA 02115, USA. NR 3 TC 12 Z9 12 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAR 20 PY 1996 VL 12 IS 5 BP 459 EP 460 DI 10.1089/aid.1996.12.459 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA UA592 UT WOS:A1996UA59200026 PM 8882333 ER PT J AU Boyce, FM Bucher, NLR AF Boyce, FM Bucher, NLR TI Baculovirus-mediated gene transfer into mammalian cells SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE xenovector; liver; gene therapy ID BETA-GALACTOSIDASE; INSECT CELLS; EXPRESSION; VIRUS; REPLICATION; VECTORS; MARKER; LINES AB This paper describes the use of the baculovirus Arctographa californica multiple nuclear polyhedrosis virus (AcMNPV) as a vector for gene delivery into mammalian cells, A modified AcMNPV virus was prepared that carried the Escherichia coli lacZ reporter gene under control of the Rous sarcoma virus promoter and mammalian RNA processing signals, This modified baculovirus was then used to infect a variety of mammalian cell lines, After infection of the human liver cell lines HepG2, >25% of the cells showed high-level expression of the transduced gene, Over 70% of the cells in primary cultures of rat hepatocytes showed expression of beta-galactosidase after exposure to the virus, Cell lines from other tissues showed less or no expression of lacZ after exposure to the virus, The block to expression in less susceptible cells does not appear to result from the ability to be internalized by the target cell but rather by events subsequent to viral entry, The onset of lacZ expression occurred within 6 hr of infection in HepG2 cells and peaked 12-24 hr postinfection, Because AcMNPV is able to replicate only in insect hosts, is able to carry large (>1.5 kb) inserts, and is a highly effective gene delivery vehicle for primary cultures of hepatocytes, AcMNPV may be a useful vector for genetic manipulation of liver cells. C1 BOSTON UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02118. RP Boyce, FM (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,BLDG 149,13TH ST,BOSTON,MA 02129, USA. FU NCI NIH HHS [CA39099] NR 22 TC 326 Z9 358 U1 1 U2 14 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 1996 VL 93 IS 6 BP 2348 EP 2352 DI 10.1073/pnas.93.6.2348 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UB121 UT WOS:A1996UB12100021 PM 8637876 ER PT J AU DeYoe, EA Carman, GJ Bandettini, P Glickman, S Wieser, J Cox, R Miller, D Neitz, J AF DeYoe, EA Carman, GJ Bandettini, P Glickman, S Wieser, J Cox, R Miller, D Neitz, J TI Mapping striate and extrastriate visual areas in human cerebral cortex SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID CORTICAL CONNECTIONS; MACAQUE; ORGANIZATION; MONKEY; COLOR AB Functional magnetic resonance imaging (fMRI) was used to identify and map the representation of the visual field in seven areas of human cerebral cortex and to identify at least two additional visually responsive regions. The cortical locations of neurons responding to stimulation along the vertical or horizontal visual field meridia were charted on three-dimensional models of the cortex and on unfolded maps of the cortical surface, These maps were used to identify the borders among areas that would be topographically homologous to areas V1, V2, V3, VP, and parts of V3A and V4 of the macaque monkey, Visually responsive areas homologous to the middle temporal/medial superior temporal area complex and unidentified parietal visual areas were also observed, The topography of the visual areas identified thus far is consistent with the organization in macaque monkeys, However, these and other findings suggest that human and simian cortical organization may begin to differ in extrastriate cortex at, or beyond, V3A and V4. C1 MED COLL WISCONSIN,BIOPHYS RES INST,MILWAUKEE,WI 53226. MASSACHUSETTS GEN HOSP,NMR CTR,BOSTON,MA 02129. SALK INST BIOL STUDIES,LA JOLLA,CA 92037. BROWN UNIV,PROVIDENCE,RI 02912. RP DeYoe, EA (reprint author), MED COLL WISCONSIN,DEPT CELLULAR BIOL & ANAT,8701 WATERTOWN PLANK RD,MILWAUKEE,WI 53226, USA. RI Bandettini, Peter/F-5871-2012 FU NEI NIH HHS [EY01931, EY10244]; NIMH NIH HHS [MH51358] NR 31 TC 701 Z9 702 U1 5 U2 26 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 19 PY 1996 VL 93 IS 6 BP 2382 EP 2386 DI 10.1073/pnas.93.6.2382 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA UB121 UT WOS:A1996UB12100027 PM 8637882 ER PT J AU Shapiro, GI Rollins, BJ AF Shapiro, GI Rollins, BJ TI p16(INK4A) as a human tumor suppressor SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER LA English DT Review ID DELETIONS; INHIBITION; MELANOMA; KINASES; P21 C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. NR 59 TC 45 Z9 45 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-419X J9 BBA-REV CANCER JI Biochim. Biophys. Acta-Rev. Cancer PD MAR 18 PY 1996 VL 1242 IS 3 BP 165 EP 169 DI 10.1016/0304-419X(95)00011-4 PG 5 WC Biochemistry & Molecular Biology; Biophysics; Oncology SC Biochemistry & Molecular Biology; Biophysics; Oncology GA UE610 UT WOS:A1996UE61000001 PM 8603068 ER PT J AU Ewen, ME Miller, SJ AF Ewen, ME Miller, SJ TI p53 and translational control SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER LA English DT Review ID CELLULAR TUMOR-ANTIGEN; INITIATION FACTOR-II; MESSENGER-RNAS; PROTEIN-SYNTHESIS; RIBOSOMAL-RNA; GROWTH-FACTOR; 3T3 CELLS; WILD-TYPE; TGF-BETA; INHIBITION AB The tumor suppressor p53 plays a role in mediating a G1 arrest (for example, in response to DNA damage), in the cellular commitment to apoptosis and in suppression of transformation. The mechanism of action of p53 in each of these biological outcomes is likely to be overlapping. Current data indicate that p53 functions as a sequence specific transcriptional activator. p53 can also repress transcription from certain promoters. One way in which p53 mediates a G1 arrest after DNA damage appears to be clear. Cells exposed to ionizing radiation show elevated levels of p53 protein. The increase in p53 levels is thought to be responsible for the increase in the cyclin-dependent kinase (cdk) inhibitor p21 mediated through the p53 binding sites in the p21 promoter. With regard to the ability of p53 to suppress transformation, there is data suggesting that p53 functions other than, or in addition to, its transcriptional activation function may be necessary [1,2]. Similar data exist for p53-dependent apoptosis [3-5]. Recently a role for p53 at another level of gene regulation, namely, translational regulation has been proposed. p53 associates with various components of the translation machinery and has been implicated in the translational regulation of both the p53 and CDK4 mRNAs. Here we will summarize the evidence suggesting a role for p53 in translation and how this regulation might be achieved. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP Ewen, ME (reprint author), HARVARD UNIV,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 48 TC 47 Z9 48 U1 0 U2 2 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-419X J9 BBA-REV CANCER JI Biochim. Biophys. Acta-Rev. Cancer PD MAR 18 PY 1996 VL 1242 IS 3 BP 181 EP 184 DI 10.1016/0304-419X(95)00010-D PG 4 WC Biochemistry & Molecular Biology; Biophysics; Oncology SC Biochemistry & Molecular Biology; Biophysics; Oncology GA UE610 UT WOS:A1996UE61000004 PM 8603071 ER PT J AU Hoeppner, DJ Hengartner, MO Fisher, DE AF Hoeppner, DJ Hengartner, MO Fisher, DE TI Programmed cell death: From development to disease SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP Hoeppner, DJ (reprint author), COLD SPRING HARBOR LAB,POB 100,COLD SPRING HARBOR,NY 11724, USA. RI Hengartner, Michael/A-7058-2008; Hengartner, Michael/E-6235-2011; OI Hengartner, Michael/0000-0002-7584-596X NR 0 TC 8 Z9 8 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-419X J9 BBA-REV CANCER JI Biochim. Biophys. Acta-Rev. Cancer PD MAR 18 PY 1996 VL 1242 IS 3 BP 217 EP 220 DI 10.1016/0304-419X(95)00017-A PG 4 WC Biochemistry & Molecular Biology; Biophysics; Oncology SC Biochemistry & Molecular Biology; Biophysics; Oncology GA UE610 UT WOS:A1996UE61000008 PM 8603075 ER PT J AU Melnik, G AF Melnik, G TI Value of specialty intravenous amino acid solutions SO AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY LA English DT Article ID PARENTERAL-NUTRITION SUPPORT; DOUBLE-BLIND TRIAL; INJURED PATIENTS; HEPATIC-ENCEPHALOPATHY; NITROGEN-RETENTION; SEPTIC PATIENTS; PROTEIN; STRESS; SUPPLEMENTATION; ENRICHMENT C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,COLL PHARM,AUSTIN,TX 78712. RP Melnik, G (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,CLIN PHARM PROGAMS,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 29 TC 0 Z9 2 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 1079-2082 J9 AM J HEALTH-SYST PH JI Am. J. Health-Syst. Pharm. PD MAR 15 PY 1996 VL 53 IS 6 BP 671 EP 674 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UA074 UT WOS:A1996UA07400012 PM 8800975 ER PT J AU Schumann, RR Nakarai, T Gruss, HJ Brach, MA vonArnim, U Kirschning, C Karawajew, L Ludwig, WD Renauld, JC Ritz, J Herrmann, F AF Schumann, RR Nakarai, T Gruss, HJ Brach, MA vonArnim, U Kirschning, C Karawajew, L Ludwig, WD Renauld, JC Ritz, J Herrmann, F TI Transcript synthesis and surface expression of the interleukin-2 receptor (alpha-, beta-, and gamma-chain) by normal and malignant myeloid cells SO BLOOD LA English DT Article ID COLONY-STIMULATING FACTOR; NF-KAPPA-B; IL-2 RECEPTOR; FUNCTIONAL COMPONENT; MONOCYTES; BINDING; FIBROBLASTS; ACTIVATION AB Expression of the interleukin-2 receptor alpha-(IL-2R alpha-), IL-2R beta-, and the recently identified IL-2R gamma-chain was examined on a wide range of cells of myeloid origin including neutrophils, monocytes, normal bone marrow-derived myeloid progenitors enriched for CD34(+) cells, bone marrow blasts obtained from acute myelogenous leukemia (AML) patients, and permanent myeloid leukemia cell lines by reverse transcriptase-polymerase chain reaction and surface membrane analysis using receptor chain-specific monoclonal antibodies and flow cytometry. Expression of the p75 IL-2R beta- and the p64 IL-2R gamma-chain was a common finding in most of the myeloid cell samples investigated, whereas IL-2R alpha-chain was less frequently expressed. Although the high-affinity IL-2R form (ie, the alpha+, beta+, gamma+ IL-2R form) was detectable in a small minority of primary AML samples as well as the KG-1 cell line and IL-2 binding to these cells was sufficient to initiate signal transduction as evidenced by an increase in overall protein tyrosine phosphorylation and more specifically in tyrosine phosphorylation of the Janus kinase (JAK) 3, in none of these cell types did exposure to IL-2 affect cell growth kinetics. These results suggest that, in myeloid cells, the IL-2R may not stimulate mitogenic responses or that its components may be expressed in a combinational association with receptors for other cytokines and that IL-2R gamma may play a regulatory role in normal and malignant myelopoiesis possibly independent from IL-2. Because recent studies by others have indicated that the IL-2R gamma- chain may be shared by the IL-4R, the IL-7R, and most likely the IL-9R, expression of mRNA of these receptor types was also investigated in these cell samples. Surprisingly, in a substantial part of the myeloid lineage cells examined, an IL-2R gamma(+), IL-4R(-). IL-7R(-) configuration was noted that was, however, frequently associated with expression of IL-9R. Sharing of IL-9R/IL-2R components was furthermore suggested by inhibition of I-125-IL-2 binding to primary AML cells with excess of unlabeled IL-9. (C) 1996 by The American Society of Hematology. C1 HUMBOLDT UNIV BERLIN,ROBERT ROSSLE CANC CTR,DEPT MED ONCOL & APPL MOLEC BIOL,D-13122 BERLIN,GERMANY. MAX DELBRUCK CTR MOLEC MED,BERLIN,GERMANY. LUDWIG INST CANC RES,BRUSSELS,BELGIUM. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA 41619] NR 37 TC 23 Z9 23 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 1996 VL 87 IS 6 BP 2419 EP 2427 PG 9 WC Hematology SC Hematology GA UA957 UT WOS:A1996UA95700035 PM 8630406 ER PT J AU Schnitt, SJ Hayman, J Gelman, R Eberlein, TJ Love, SM Mayzel, K Osteen, RT Nixon, AJ Pierce, S Connolly, JL Cohen, P Schneider, L Silver, B Recht, A Harris, JR AF Schnitt, SJ Hayman, J Gelman, R Eberlein, TJ Love, SM Mayzel, K Osteen, RT Nixon, AJ Pierce, S Connolly, JL Cohen, P Schneider, L Silver, B Recht, A Harris, JR TI A prospective study of conservative surgery alone in the treatment of selected patients with stage I breast cancer SO CANCER LA English DT Article DE breast cancer; conservative surgery ID RANDOMIZED CLINICAL-TRIAL; TERM FOLLOW-UP; RADIATION-THERAPY; SEGMENTAL-MASTECTOMY; AXILLARY DISSECTION; CONSERVING SURGERY; RADIOTHERAPY; LUMPECTOMY; RECURRENCE; IRRADIATION AB BACKGROUND. Randomized clinical trials have clearly demonstrated that the use of radiation therapy (RT) following breast-conserving surgery (CS) substantially reduces the risk of local recurrence. However, the low rate of local recurrence after CS and RT for patients without known risk factors, and the recent increase in the detection of smaller cancers due to mammographic screening have led to the speculation that a subgroup of patients who have a low risk of local recurrence without RT might be identified. In 1986, we initiated a one-arm, prospective clinical trial of CS alone for treatment of highly selected breast patients without known risk factors for local recurrence. METHODS. The study had a sequential design with a planned accrual of 90 patients. Criteria for entry into the trial were: a unicentric, clinical T1 infiltrating ductal, mucinous or tubular carcinoma without an extensive intraductal component or lymphatic vessel invasion; a wide excision with a pathologically-documented negative margin of at least 1 cm; and histologically negative axillary lymph nodes. No adjuvant RT or systemic therapy was administered. Seventy-six per cent of the lesions were detected by mammography alone. The median gross pathologic tumor size was 0.9 cm. The median patient age was 67 years. RESULTS. Eighty-seven patients were enrolled in the trial before it closed prematurely in 1992 because the predefined stopping boundary was crossed (i.e., the sixth local recurrence was observed). At that time, the average annual local recurrence rate was 4.2%. With a median follow-up of 56 months, there are now 14 patients (165) with local recurrence as their site of first failure (average annual local recurrence rate: 3.6%). Four patients without local recurrence developed distant metastases. Three patients have died, one of metastatic breast cancer and tow of unrelated causes. CONCLUSIONS. Even in a highly selected group of patients with early-stage breast cancer, there is a substantial risk of early local recurrence for those treated with wide excision alone. (C) 1996 American Cancer Society. C1 HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT SURG SURG ONCOL,BOSTON,MA 02115. DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. FAULKNER HOSP,FAULKNER BREAST CTR,BOSTON,MA. RP Schnitt, SJ (reprint author), BETH ISRAEL HOSP,DEPT PATHOL,330 BROOKLINE AVE,BOSTON,MA 02215, USA. NR 24 TC 91 Z9 93 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAR 15 PY 1996 VL 77 IS 6 BP 1094 EP 1100 DI 10.1002/(SICI)1097-0142(19960315)77:6<1094::AID-CNCR14>3.3.CO;2-J PG 7 WC Oncology SC Oncology GA TY621 UT WOS:A1996TY62100014 PM 8635129 ER PT J AU Barker, FG Davis, RL Chang, SM Prados, MD AF Barker, FG Davis, RL Chang, SM Prados, MD TI Necrosis as a prognostic factor in glioblastoma multiforme SO CANCER LA English DT Article DE glioblastoma multiforme; anaplastic astrocytoma; necrosis; survival analysis; prognostic factors ID ANAPLASTIC ASTROCYTOMA; HISTOLOGIC FEATURES; GRADING SYSTEM; GLIOMAS; SURVIVAL; DIAGNOSIS; SUPRATENTORIAL; SURGERY; TRIALS AB BACKGROUND. Many pathologists require the presence of tumor necrosis within an astrocytic neoplasm to establish the diagnosis of glioblastoma multiforme (GM). Two new grading systems for astrocytic neoplasms allow a tumor to be diagnosed at the highest level of anaplasia without requiring the presence of tumor necrosis. METHODS. To determine whether GMs without necrosis had biologic behavior most compatible with a diagnosis pf GM or of anaplastic astrocytoma (AA), we examined the survival of 299 patients whose tumors were diagnosed as GM because they contained endothelial proliferation and who were treated according to prospective clinical protocols. Multivariate proportional-hazards survival analysis was used to assess the importance of tumor necrosis after adjustment for other prognostic factors. RESULTS. Of 275 patients with GMs containing endothelial proliferation, 88% had tumor necrosis. Absence of necrosis was associated with younger age and with less extensive surgical resection. The absence of necrosis predicted longer survival in univariate analysis (P = 0.02) and after adjustment for age, Karnofsky performance score, and extent of resection in a multivariate analysis (P = 0.04). However, the magnitude of the survival difference was not clinically important: patients without tumor necrosis had a median survival of 12.5 months, and those with tumor necrosis had a median survival of 10.9 months. Kaplan-Meier survival rates two years after diagnosis were 13.0% for patients with necrosis and 27.1% for patients without necrosis; the difference in 2-year survival was not statistically significant (difference in survival rates = 14.1%, 95% confidence interval -2.2% to 30.4%). CONCLUSIONS. The survival of patients with astrocytic neoplasms containing endothelial proliferation and no necrosis conforms best to the pattern expected for patients with GM rather than AA. This supports the classification of these tumors as GM in the revised World Health Organization grading system and as grade 4 astrocytomas in the St. Anne-Mayo grading system. (C) 1996 American Cancer Society. C1 UNIV CALIF SAN FRANCISCO,DEPT NEUROL SURG,BRAIN TUMOR RES CTR,NEUROONCOL SERV,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT PATHOL,NEUROPATHOL UNIT,SAN FRANCISCO,CA. RP Barker, FG (reprint author), MASSACHUSETTS GEN HOSP,NEUROSURG SERV,WARREN 905,FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 09291, CA 13525] NR 35 TC 94 Z9 95 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAR 15 PY 1996 VL 77 IS 6 BP 1161 EP 1166 DI 10.1002/(SICI)1097-0142(19960315)77:6<1161::AID-CNCR24>3.0.CO;2-Z PG 6 WC Oncology SC Oncology GA TY621 UT WOS:A1996TY62100024 PM 8635139 ER PT J AU Gerweck, LE Seetharaman, K AF Gerweck, LE Seetharaman, K TI Cellular pH gradient in tumor versus normal tissue: Potential exploitation for the treatment of cancer SO CANCER RESEARCH LA English DT Article ID P-31 MR SPECTROSCOPY; INTRACELLULAR-PH; THERAPY; SARCOMAS AB Although limited data exist, electrode-measured pH values of human tumors and adjacent normal tissues, which are concurrently obtained by the same investigator in the same patient, consistently show that the electrode pH (believed to primarily represent tissue extracellular pH) is substantially and consistently lower in tumor than in normal tissue. In contrast, the P-31-magnetic resonance spectroscopy estimated that intracellular pH is essentially identical or slightly more basic in tumor compared to normal tissue, As a consequence, the cellular pH gradient is substantially reduced or reversed in tumor compared to normal tissue: in normal tissue the extracellular pH is relatively basic, and in tumor tissue the magnitude of the pH gradient is reduced or reversed. This difference provides an exploitable avenue for the treatment of cancer. The extent to which drugs exhibiting weakly acid or basic properties are ionized is strongly dependent on the pH of their milieu. Weakly acidic drugs which are relatively lipid soluble in their nonionized state may diffuse freely across the cell membrane and, upon entering a relatively basic intracellular compartment, become trapped and accumulate within a cell, leading to substantial differences in the intracellular/extracellular drug distribution between tumor and normal tissue for drugs exhibiting appropriate pKas. RP Gerweck, LE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,COX 302,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA22860] NR 38 TC 572 Z9 581 U1 12 U2 91 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1996 VL 56 IS 6 BP 1194 EP 1198 PG 5 WC Oncology SC Oncology GA TZ527 UT WOS:A1996TZ52700005 PM 8640796 ER PT J AU Marsh, DJ Andrew, SD Eng, C Learoyd, DL Capes, AG Pojer, R Richardson, AL Houghton, C Mulligan, LM Ponder, BAJ Robinson, BG AF Marsh, DJ Andrew, SD Eng, C Learoyd, DL Capes, AG Pojer, R Richardson, AL Houghton, C Mulligan, LM Ponder, BAJ Robinson, BG TI Germline and somatic mutations in an oncogene: RET mutations in inherited medullary thyroid carcinoma SO CANCER RESEARCH LA English DT Article ID ENDOCRINE NEOPLASIA TYPE-2A; CANCER AB Inherited cancer syndromes predispose an individual to the development of specific tumors. Somatic and germline mutations in the same tumor suppressor gene, as described in Knudson's two-mutation model, are well recognized. Inherited mutations in the RET proto-oncogene, which encodes a receptor tyrosine kinase, predispose individuals to the multiple endocrine neoplasia type 2 (MEN 2) cancer syndromes. The major component tumor of these syndromes is medullary thyroid carcinoma (MTC). To date, somatic mutations in RET have not been identified in tumors from individuals with MEN 2, although they have been well documented in sporadic MEN 2-related tumors. We have identified, among 16 MEN 2 cases with well-defined RET germline mutations, a somatic missense mutation at codon 918 of RET in 3 of 15 MTCs and in a sample with hyperplastic C-cells (the presumed precursor to hereditary MTC). We suggest that the presence of a somatic mutation, in addition to the preexisting germline mutation in hereditary MTCs, may contribute to tumorigenesis in vivo. C1 ROYAL N SHORE HOSP,KOLLING INST MED RES,ST LEONARDS,NSW 2065,AUSTRALIA. ROYAL N SHORE HOSP,DEPT ENDOCRINOL,ST LEONARDS,NSW 2065,AUSTRALIA. UNIV SYDNEY,SYDNEY,NSW 2006,AUSTRALIA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. UNIV CAMBRIDGE,ADDENBROOKES HOSP,CANC RES CAMPAIGN,HUMAN CANC GENET RES GRP,CAMBRIDGE CB2 2QQ,ENGLAND. QUEENS UNIV,DEPT PEDIAT,KINGSTON,ON K7L 3N6,CANADA. QUEENS UNIV,DEPT PATHOL,KINGSTON,ON K7L 3N6,CANADA. RI Marsh, Deborah/I-1491-2014; OI Marsh, Deborah/0000-0001-5899-4931; Eng, Charis/0000-0002-3693-5145 NR 30 TC 48 Z9 49 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1996 VL 56 IS 6 BP 1241 EP 1243 PG 3 WC Oncology SC Oncology GA TZ527 UT WOS:A1996TZ52700015 PM 8640806 ER PT J AU Chen, L Waxman, DJ Chen, DS Kufe, DW AF Chen, L Waxman, DJ Chen, DS Kufe, DW TI Sensitization of human breast cancer cells to cyclophosphamide and ifosfamide by transfer of a liver cytochrome P450 gene SO CANCER RESEARCH LA English DT Article ID HUMAN ADENOVIRUS TYPE-5; INDUCED RAT-LIVER; CYTOSINE DEAMINASE; MUC1 GENE; METABOLISM; INVIVO; ACTIVATION; TUMORS; DNA; 5-FLUOROCYTOSINE AB The cancer chemotherapeutic agent cyclophosphamide (CPA) and its isomer ifosfamide (IFA) are alkylating agent prodrugs that require metabolism by liver cytochrome P450 (P350) enzymes for antitumor activity. The therapeutic effectiveness of these oxazaphosphorines is limited by the hematopoietic, renal, and cardiac toxicity that accompanies the systemic distribution of liver-derived activated drug metabolites. Transfer of a liver cytochrome P450 gene, CYP2B1, into human breast MCF-7 cancer cells is presently shown to greatly sensitize these cells to oxazaphosphorine toxicity as a consequence of the acquired capacity for intratumoral CPA and IFA activation. Thus, CPA and IFA were highly cytotoxic to MCF-7 cells following stable transfection of CYP2B1 but exhibited no toxicity to parental tumor cells or to a beta-galactosidase-expressing MCF-7 transfectant. This cytotoxicity could be appreciably blocked by the CYP2B1 inhibitor metyrapone. Cell cycle analysis revealed that CPA arrested the CYP2B1-expressing cells, but not CYP2B1-negative cells, at G(2)-M phase. A strong bystander cytotoxicity effect that does not require direct cell-cell contact was mediated by CYP2B1-expressing MCF-7 cells on non-CYP2B1 cells. Intratumoral CYP2B1 expression conferred a distinct therapeutic advantage when treating MCF-7 tumors grown in nude mice with CPA, as revealed by a 15-20-fold greater in vivo cytotoxicity, determined by tumor excision/colony formation assay, and by the substantially enhanced antitumor activity, monitored by tumor growth delay, for CYP2B1-expressing MCF-7 tumors as compared to CYP2B1-negative control tumors. These enhanced therapeutic effects were obtained without any apparent increase in host toxicity. To evaluate the extent to which a CPA/P450 gene therapy strategy may be generally applicable to other tumor cell types, a replication-defective recombinant adenovirus carrying the CYP2B1 gene driven by the cytomegalovirus (CMV) promoter Ad.CMV-2B1 was constructed and used to infect a panel of human tumor cell lines. Ad.CMV-2B1 infection rendered each of the cell lines highly sensitive to CPA and IFA cytotoxicity, with substantial chemosensitization seen at multiplicities of infection as low as 10. The CPA/P450 prodrug activation system may thus serve as a useful paradigm for further development of novel cancer gene therapy strategies that utilize drug susceptibility genes to significantly potentiate the antitumor activity of conventional cancer chemotherapeutic agents. C1 BOSTON UNIV,DEPT BIOL,DIV CELL & MOLEC BIOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [CA49248] NR 61 TC 86 Z9 91 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1996 VL 56 IS 6 BP 1331 EP 1340 PG 10 WC Oncology SC Oncology GA TZ527 UT WOS:A1996TZ52700031 PM 8640822 ER PT J AU Stegmaier, K Takeuchi, S Golub, TR Bohlander, SK Bartram, CR Koeffler, HP Gilliland, DG AF Stegmaier, K Takeuchi, S Golub, TR Bohlander, SK Bartram, CR Koeffler, HP Gilliland, DG TI Mutational analysis of the candidate tumor suppressor genes TEL and KIP1 in childhood acute lymphoblastic leukemia SO CANCER RESEARCH LA English DT Article ID HUMAN DNA; RETINOBLASTOMA; CANCER AB We have shown previously that loss of heterozygosity at chromosome band 12p13 is among the most frequent genetic abnormalities identified in acute lymphoblastic leukemia (ALL) of childhood. Two known genes map within the critically deleted region of 12p: TEL, the gene encoding a new member of the ETS family of transcription factors, which is rearranged in a variety of hematological malignancies; and KIP1, the gene encoding the cyclin-dependent kinase inhibitor p27. Both genes are, therefore, excellent candidate tumor suppressor genes. In this report, we determined the exon organization of the TEL gene and performed mutational analysis of TEL and KIP1 in 33 childhood ALL patients known to have loss of heterozygosity at this locus. No mutations in either TEL or KIP1 were found; this suggests that neither TEL nor KIP1 is the critical 12p tumor suppressor gene in childhood ALL. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. UNIV CALIF LOS ANGELES,SCH MED,CEDARS SINAI RES INST,DIV HEMATOL ONCOL,LOS ANGELES,CA 90048. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV CHICAGO,HEMATOL ONCOL SECT,CHICAGO,IL 60637. UNIV ULM,DEPT PEDIAT 2,MOLEC BIOL SECT,D-89081 ULM,GERMANY. OI Bohlander, Stefan/0000-0002-2202-9088 FU NCI NIH HHS [CA42710, CA57261]; NIDDK NIH HHS [DK42792] NR 38 TC 75 Z9 77 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1996 VL 56 IS 6 BP 1413 EP 1417 PG 5 WC Oncology SC Oncology GA TZ527 UT WOS:A1996TZ52700042 PM 8640833 ER PT J AU Lomo, LC Motte, RW Giraldo, AA Nabozny, GH David, CS Rimm, IJ Kong, YCM AF Lomo, LC Motte, RW Giraldo, AA Nabozny, GH David, CS Rimm, IJ Kong, YCM TI V beta 8.2 transgene expression interferes with development of experimental autoimmune thyroiditis in CBA k/q but not k/k mice SO CELLULAR IMMUNOLOGY LA English DT Article ID T-CELL RECEPTORS; BETA-SPECIFIC ANTIBODIES; MOUSE THYROGLOBULIN; SHARED DETERMINANTS; RESPONDER MICE; SELF-TOLERANCE; GENE USAGE; MURINE; ENCEPHALOMYELITIS; INDUCTION AB The thyroiditogenic T cell receptor (TCR) repertoire is not yet well defined in murine experimental autoimmune thyroiditis (EAT), Our recent work has shown that, while V beta 8(+) T cells have no major role in EAT induction with mouse thyroglobulin (MTg), V beta 13 may be involved, To examine the effect of skewing the TCR repertoire on EAT development, CBA (H2(k)) mice were mated with B10.Q mice harboring an ovalbumin-specific V beta 8.2 TCR transgene (trg), and the trg(+) mice were backcrossed to CBA, FAGS analysis showed that peripheral blood T cells from trg(+) mice had about 76 and 90% V beta 8.2(+) cells in the CD4(+) and CD8(+) subsets, respectively, compared with about 15 and 11% in trg(-) sibs, The transgenic CBA Wk and k/q mice were immunized with MTg and sacrificed 28 days later, In all trg(+) mice, anti-MTg titers and T cell proliferative responses to MTg were significantly lowered, However, thyroid infiltration was distinctly different in the two strains of transgenic mice; a significant decrease was seen primarily in k/q, but not Mk, trg(+) mice. Thus, skewing the TCR repertoire to overexpress an irrelevant TCR revealed the possession of a less flexible thyroiditogenic TCR repertoire in k/q, but not k/k, mice. (C) 1996 Academic Press, Inc. C1 WAYNE STATE UNIV,SCH MED,DEPT IMMUNOL & MICROBIOL,DETROIT,MI 48201. MAYO CLIN,DEPT IMMUNOL,ROCHESTER,MN. DANA FARBER CANC INST,DEPT PEDIAT,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. ST JOHN HOSP & MED CTR,DIV IMMUNOPATHOL,DETROIT,MI 48201. FU NIDDK NIH HHS [DK 45960] NR 32 TC 10 Z9 10 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD MAR 15 PY 1996 VL 168 IS 2 BP 297 EP 301 DI 10.1006/cimm.1996.0079 PG 5 WC Cell Biology; Immunology SC Cell Biology; Immunology GA UA413 UT WOS:A1996UA41300022 PM 8640878 ER PT J AU Hamdan, AD Quist, WC Gagne, JB Feener, EP AF Hamdan, AD Quist, WC Gagne, JB Feener, EP TI Angiotensin-converting enzyme inhibition suppresses plasminogen activator inhibitor-1 expression in the neointima of balloon-injured rat aorta SO CIRCULATION LA English DT Article DE plasminogen; angiotensin; aorta; balloon; catheterization ID GENE-EXPRESSION; MYOCARDIAL-INFARCTION; VASCULAR INJURY; PROLIFERATION; ANGIOPLASTY; ARTERIAL; SYSTEM; INVIVO; GROWTH; RISK AB Background Plasminogen activator inhibitor-1 (PAI-1), an important regulator of fibrinolysis and extracellular matrix turnover, has been implicated in a number of vascular diseases. Studies demonstrating angiotensin II (Ang II) to be a potent stimulator of PAI-1 expression in cultured vascular cells suggests that the renin-angiotensin system may modulate vascular PAI-1 expression. Methods and Results We examined the effects of the ACE inhibitor captopril on PAI-1 expression in control and balloon-injured rat aorta. Northern blot analysis demonstrated that aortic PAI-1 mRNA expression was 7.6-fold elevated 3 hours (P<.05) after balloon injury, back to baseline at 2 days, increased again at 4 days, and by 7 days after balloon injury was 3.2-fold elevated (P<.05) when compared with control. In captopril-treated rats, the induction of PAI-1 expression by balloon injury was significantly suppressed by 44% (P<.05) in the 7-day group but was not altered in the 3-hour group. Captopril also reduced baseline aortic PAI-1 mRNA. In situ hybridization and immunohistochemistry revealed dense PAI-1 staining of 7-day neointima in untreated rats and a dramatic decrease in PAI-1 in neointima of captopril-treated rats. Conclusions This report demonstrates that balloon injury results in both a rapid ACE inhibitor-independent induction of aortic PAI-1 expression and a later increase in PAI-1 in the neointima that is significantly suppressed by captopril. This provides the first evidence that the renin-angiotensin system regulates neointimal PAI-1 expression and that ACE inhibitors can reduce PAI-1 in the vessel wall in vivo. C1 JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT VASC SURG,BOSTON,MA 02215. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02215. FU BHP HRSA HHS [DH48358]; NHLBI NIH HHS [T32HL07734-02]; NIDDK NIH HHS [P30 DK036836]; PHS HHS [36836] NR 30 TC 86 Z9 91 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR 15 PY 1996 VL 93 IS 6 BP 1073 EP 1078 PG 6 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA UA053 UT WOS:A1996UA05300003 PM 8653825 ER PT J AU Albert, CM McGovern, BA Newell, JB Ruskin, JN AF Albert, CM McGovern, BA Newell, JB Ruskin, JN TI Sex differences in cardiac arrest survivors SO CIRCULATION LA English DT Article DE death, sudden; women; arrhythmia; electrophysiology; fibrillation ID MYOCARDIAL-INFARCTION; SUDDEN-DEATH; GENDER; WOMEN; INDUCIBILITY; DISEASE; RISK AB Background Important sex differences in the epidemiology of sudden death and in the results of electrophysiological testing in survivors of cardiac arrest have been identified. These differences are currently poorly understood. Methods and Results Three hundred fifty-five consecutive survivors of out-of-hospital cardiac arrest (84 women and 271 men) referred for electrophysiologically guided therapy were analyzed retrospectively for sex differences in underlying pathology and predictors of outcome. Women were significantly less likely to have underlying coronary artery disease than men (45% versus 80%) and more likely to have other forms of heart disease or structurally normal hearts (P<.0001). The mean left ventricular ejection fraction was higher in women (0.46+/-0.18 versus 0.41+/-0.18, P<.05), and women were more likely to have no inducible arrhythmia at baseline electrophysiological testing (46% versus 27%, P=.002), although when the patients were stratified by coronary artery disease status, these sex differences were no longer present. The independent predictors of outcome differed between men and women. In men, a left ventricular ejection fraction of <0.40 was the most powerful independent predictor of total (relative risk, 2.8; 95% CI, 1.6 to 5.0; P<.0001) and cardiac (relative risk, 6.3; 95% CI, 2.9 to 13.5; P<.0001) mortality. In contrast, the presence of coronary artery disease was the only independent predictor of total (relative risk, 4.5; 95% CI, 1.5 to 13.4; P=.003) and cardiac (relative risk, 4.4; 95% CI, 1.2 to 15.6; P=.012) mortality in women. Conclusions Female survivors of cardiac arrest are less likely to have underlying coronary artery disease. The predictors of total and cardiac mortality differ between male and female survivors. Coronary artery disease status is the most important predictor in women, and impaired left ventricular function is the most important predictor in men. C1 MASSACHUSETTS GEN HOSP,CARDIAC ARRHYTHMIA SERV,BOSTON,MA 02114. NR 15 TC 110 Z9 112 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR 15 PY 1996 VL 93 IS 6 BP 1170 EP 1176 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA UA053 UT WOS:A1996UA05300016 PM 8653838 ER PT J AU Brezinski, ME Tearney, GJ Bouma, BE Izatt, JA Hee, MR Swanson, EA Southern, JF Fujimoto, JG AF Brezinski, ME Tearney, GJ Bouma, BE Izatt, JA Hee, MR Swanson, EA Southern, JF Fujimoto, JG TI Optical coherence tomography for optical biopsy - Properties and demonstration of vascular pathology SO CIRCULATION LA English DT Article DE atherosclerosis; lasers; imaging ID CORONARY-ARTERY DISEASE; MYOCARDIAL-INFARCTION; BIOLOGICAL TISSUES; REFLECTOMETRY; ANGIOGRAPHY; ANGIOSCOPY; LIGHT AB Background Optical coherence tomography (OCT) is a recently developed medical diagnostic technology that uses back-reflected infrared light to perform in situ micron scale tomographic imaging. In this work, we investigate the ability of OCT to perform micron scale tomographic imaging of the internal microstructure of in vitro atherosclerotic plaques. Methods and Results Aorta and relevant nonvascular tissue were obtained at autopsy. Two-dimensional cross-sectional imaging of the exposed surface of the arterial segments was performed in vitro with OCT. A 1300-nm wavelength, super-luminescent diode light source was used that allows an axial spatial resolution of 20 mu m. The signal-to-noise ratio was 109 dB. Images were displayed in gray scale or false color, Imaging was performed over 1.5 mm into heavily calcified tissue, and a high contrast was noted between lipid- and water-based constituents, making OCT attractive for intracoronary imaging. The 20-mu m axial resolution of OCT allowed small structural details such as the width of intimal caps and the presence of fissures to be determined. The extent of lipid collections, which had a low backscattering intensity, also were well documented. Conclusions OCT represents a promising new technology for imaging Vascular microstructure with a level of resolution not previously achieved with the use of other imaging modalities. It does not require direct contact with the vessel wall and can be performed with a catheter integrated with a relatively inexpensive optical fiber. The high contrast among tissue constituents, high resolution, and ability to penetrate heavily calcified tissue make OCT an attractive new imaging technology for intracoronary diagnostics. C1 MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. MIT,LINCOLN LAB,LEXINGTON,MA 02173. FU NEI NIH HHS [9-RO1-EY11289-10]; NIGMS NIH HHS [9-RO1-GM35459-09] NR 42 TC 354 Z9 364 U1 1 U2 21 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR 15 PY 1996 VL 93 IS 6 BP 1206 EP 1213 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA UA053 UT WOS:A1996UA05300021 PM 8653843 ER PT J AU Camargo, CA AF Camargo, CA TI Case-control and cohort studies of moderate alcohol consumption and stroke SO CLINICA CHIMICA ACTA LA English DT Article; Proceedings Paper CT International Symposium on Health Effects of Moderate Alcohol Consumption - A Paradigmatic Risk Factor CY DEC 03-04, 1994 CL TORONTO, CANADA SP Univ Toronto, Dept Clin Biochem, Univ Toronto, Dept Nutr Sci, Hlth Canada, Coalit Responsible Drinking, Hosp Sick Children Fdn, DISCUS, MDS Labs DE alcohol drinking; cerebrovascular disorders; epidemiology ID CEREBROVASCULAR-DISEASE HOSPITALIZATIONS; RISK-FACTORS; ISCHEMIC STROKE; CIGARETTE-SMOKING; DRINKING HABITS; BRITISH MEN; MORTALITY; ASSOCIATION; HEMORRHAGE; WOMEN AB Epidemiologic evidence suggests that alcohol consumption has distinctive associations with risk of ischemic and hemorrhagic strokes; these differences help explain apparent inconsistencies in the alcohol-stroke literature (Camargo CA Jr. Stroke 1989;20:1611-1626). To better define the impact of ''moderate drinking'' per se (i.e. usual consumption of less than or equal to 2 drinks daily for men, and less than or equal to 1 drink daily for women), the present author reviewed 26 case-control and cohort studies on this subject. There is substantial evidence that moderate drinking does not increase risk of ischemic stroke; studies remain divided, however, on the question of a ''protective'' association. Furthermore, although the evidence is not unanimous, two major cohort studies have found that even moderate drinking may increase risk of hemorrhagic stroke. Because ischemic strokes are 3-4 times more common than hemorrhagic strokes, the net impact of moderate drinking on stroke risk depends greatly on the relation between moderate drinking and ischemic stroke. It is most likely, however, that moderate drinking does not increase risk of all strokes combined. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT EMERGENCY MED,BOSTON,MA. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. RP Camargo, CA (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-07575] NR 41 TC 41 Z9 41 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0009-8981 J9 CLIN CHIM ACTA JI Clin. Chim. Acta PD MAR 15 PY 1996 VL 246 IS 1-2 BP 107 EP 119 DI 10.1016/0009-8981(96)06231-6 PG 13 WC Medical Laboratory Technology SC Medical Laboratory Technology GA UB964 UT WOS:A1996UB96400009 PM 8814960 ER PT J AU SawkaVerhelle, D TartareDeckert, S White, MF vanObberghen, E AF SawkaVerhelle, D TartareDeckert, S White, MF vanObberghen, E TI Insulin receptor substrate-2 binds to the insulin receptor through its phosphotyrosine-binding domain and through a newly identified domain comprising amino acids 591-786 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IRS-1; PROTEIN; CELLS AB We compared the interaction between the insulin receptor (IR) and the IR substrate (IRS) proteins (IRS-1 and IRS-2) using the yeast two hybrid system. Both IRS proteins interact specifically with the cytoplasmic portion of the IR and the related insulin-like growth factor-I receptor, and these interactions require receptor tyrosine kinase activity. Alignment of IRS-1 and IRS-2 revealed two conserved domains at the NH2 terminus, called IH1(PH) and IH2(PTB), which resemble a pleckstrin homology (PH) domain and a phosphotyrosine binding (PTB) domain, respectively. The IH2(PTB) binds to the phosphorylated NPXY motif (Tyr-960) in the activated insulin receptor, providing a specific mechanism for the interaction between the receptor and IRS-1. Although the IH2(PTB) of IRS-2 also interacts with the NPEY motif of the insulin receptor, it is not essential for the inter action between the insulin receptor and IRS-2 in the yeast two-hybrid system. IRS-2 contains another interaction domain between residues 591 and 786, which is absent in IRS-1. This IRS-2-specific domain is independent of the IH2(PTB) and does not require the NPEY motif; however, it requires a functional insulin receptor kinase and the presence of three tyrosine phosphorylation sites in the regulatory loop (Tyr-1146, Tyr-1150, and Tyr-1151). Importantly, this novel domain mediates the association between IRS-2 and insulin receptor lacking the NPXY motif and may provide a mechanism by which the stoichiometry of regulatory loop autophosphorylation enhances IRS-2 phosphorylation. C1 FAC MED NICE,INSERM,U145,F-06107 NICE 2,FRANCE. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02215. RI TARTARE-DECKERT, Sophie/P-6057-2015 OI TARTARE-DECKERT, Sophie/0000-0001-8680-5720 FU NIDDK NIH HHS [DK 38712, DK 43808] NR 30 TC 140 Z9 141 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1996 VL 271 IS 11 BP 5980 EP 5983 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UA363 UT WOS:A1996UA36300008 PM 8626379 ER PT J AU Premont, RT Macrae, AD Stoffel, RH Chung, NJ Pitcher, JA Ambrose, C Inglese, J MacDonald, ME Lefkowitz, RJ AF Premont, RT Macrae, AD Stoffel, RH Chung, NJ Pitcher, JA Ambrose, C Inglese, J MacDonald, ME Lefkowitz, RJ TI Characterization of the G protein-coupled receptor kinase GRK4 - Identification of four splice variants SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUNTINGTONS-DISEASE GENE; BETA-GAMMA-SUBUNITS; RHODOPSIN KINASE; FAMILY; REGION; ISOPRENYLATION; MEMBER AB A novel human G protein-coupled receptor kinase was recently identified by positional cloning in the search for the Huntington's disease locus (Ambrose, C., James, M., Barnes, G., Lin, C., Bates, G., Altherr, M., Duyao, M., Groot, N., Church, D., Wasmuth, J. J., Lehrach, H., Housman, D., Buckler, A., Gusella, J. F., and MacDonald, M. E. (1993) Hum. Mel. Genet. 1, 697-703). Comparison off the deduced amino acid sequence of GRK4 with those of the closely related GRK5 and GRK6 suggested the apparent loss of 32 codons in the amino-terminal domain and 46 codons in the carboxyl terminal domain of GRK4. These two regions undergo alternative splicing in the GRK4 mRNA, resulting from the presence or absence of exons filling one or both of these apparent gaps. Each inserted sequence maintains the open reading frame, and the deduced amino acid sequences are similar to corresponding regions of GRK5 and GRK6. Thus, the GRK4 mRNA and the GRK4 protein can exist as four distinct variant forms. The human GRK4 gene is composed of 16 exons extending over 75 kilobase pairs of DNA. The two alternatively spliced exons correspond to exons II and XV. The genomic organization of the GRK4 gene is completely distinct from that of the human GRK2 gene, highlighting the evolutionary distance since the divergence of these two genes. Human GRK4 mRNA is expressed highly only in testis, and both alternative exons are abundant in testis mRNA. The four GRK4 proteins have been expressed, and all incorporate [H-3]palmitate. GRK4 is capable of augmenting the desensitization of the rat luteinizing hormone/chorionic gonadotropin receptor upon coexpression in HEK293 cells and of phosphorylating the agonist-occupied, purified beta(3)-adrenergic receptor, indicating that GRK4 is a functional protein kinase. C1 DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT MED CARDIOL,DURHAM,NC 27710. DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT BIOCHEM,DURHAM,NC 27710. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. FU NHGRI NIH HHS [HG00169]; NHLBI NIH HHS [HL16037]; NINDS NIH HHS [NS16367] NR 39 TC 134 Z9 138 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1996 VL 271 IS 11 BP 6403 EP 6410 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA UA363 UT WOS:A1996UA36300068 PM 8626439 ER PT J AU Napoli, R Davalli, AM Hirshman, MF Weitgasser, R Weir, GC Horton, ES AF Napoli, R Davalli, AM Hirshman, MF Weitgasser, R Weir, GC Horton, ES TI Islet transplantation under the kidney capsule fully corrects the impaired skeletal muscle glucose transport system of streptozocin diabetic rats SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE GLUT4; GLUT1; intrinsic activity; translocation; fractionation procedure ID INSULIN RESISTANCE; INTRINSIC ACTIVITY; 3T3-L1 ADIPOCYTES; ADIPOSE-CELLS; SUBCELLULAR TRAFFICKING; PLASMA-MEMBRANE; GLUT4; EXPRESSION; INVIVO; TRANSLOCATION AB Chronic insulin therapy improves but does not restore impaired insulin-mediated muscle glucose uptake in human diabetes or muscle glucose uptake, transport, and transporter translocation in streptozocin diabetic rats. To determine whether this inability is due to inadequate insulin replacement, we studied fasted streptozocin-induced diabetic Lewis rats either unheated or after islet transplantation under the kidney capsule. Plasma glucose was increased in untreated diabetics and normalized by the islet transplantation (110+/-5, 452+/-9, and 102+/-3 mg/dl in controls, untreated diabetics, and transplanted diabetics, respectively). Plasma membrane and intracellular microsomal membrane vesicles were prepared from hindlimb skeletal muscle of basal and maximally insulin-stimulated rats. Islet transplantation normalized plasma membrane carrier-mediated glucose transport V-max, plasma membrane glucose transporter content, and insulin-induced transporter translocation. There were no differences in transporter intrinsic activity (V-max/R(o)) among the three groups. Microsomal membrane GLUT4 content was reduced by 30% in untreated diabetic rats and normal in transplanted diabetics, whereas the insulin-induced changes in microsomal membrane GLUT4 content were quantitatively similar in the three groups. There were no differences in plasma membrane GLUT1 among the groups and between basal and insulin stimulated states. Microsomal membrane GLUT1 content was increased 60% in untreated diabetics and normalized by the transplantation. In conclusion, an adequate insulin delivery in the peripheral circulation, obtained by islet transplantation, fully restores the muscle glucose transport system to normal in streptozocin diabetic rats. C1 JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. OI NAPOLI, Raffaele/0000-0002-3366-2321 FU NIDDK NIH HHS [DK 36836, DK-35449, R01-DK-26317] NR 68 TC 20 Z9 20 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAR 15 PY 1996 VL 97 IS 6 BP 1389 EP 1397 DI 10.1172/JCI118559 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA UB756 UT WOS:A1996UB75600007 PM 8617870 ER PT J AU LItalien, GJ Paul, SD Hendel, RC Leppo, JA Cohen, MC Fleisher, LA Brown, KA Zarich, SW Cambria, RP Cutler, BS Eagle, KA AF LItalien, GJ Paul, SD Hendel, RC Leppo, JA Cohen, MC Fleisher, LA Brown, KA Zarich, SW Cambria, RP Cutler, BS Eagle, KA TI Development and validation of a Bayesian model for perioperative cardiac risk assessment in a cohort of 1,081 vascular surgical candidates SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; DIPYRIDAMOLE-THALLIUM SCINTIGRAPHY; MYOCARDIAL-INFARCTION; LOGISTIC-REGRESSION; NONCARDIAC SURGERY; LIKELIHOOD RATIOS; CAROTID ENDARTERECTOMY; PROGNOSTIC VALUE; PREDICTIVE VALUE; MORBIDITY AB Objectives. This study sought to develop and validate a Bayesian risk prediction model for vascular surgery candidates. Background. Patients who require surgical treatment of peripheral vascular disease are at increased risk of perioperative cardiac morbidity and mortality. Existing prediction models tend to underestimate risk in vascular surgery candidates. Methods. The cohort comprised 1,081 consecutive vascular surgery candidates at five medical centers. Of these, 567 patients from two centers (''training'' set) were used to develop the model, and 514 patients from three centers were used to validate it (''validation'' set). Risk scores were developed using logistic regression for clinical variables: advanced age (>70 years), angina, history of myocardial infarction, diabetes mellitus, history of congestive heart failure and prior coronary revascularization. A second model was developed from dipyridamole-thallium predictors of myocardial infarction (i.e., fixed and reversible myocardial defects and ST changes). Model performance was assessed by comparing observed event rates with risk estimates and by performing receiver-operating characteristic curve (ROC) analysis. Results. The postoperative cardiac event rate was 8% for both sets. Prognostic accuracy (i.e., ROC area) was 74 +/- 3% (mean +/- SD) for the clinical and 81 +/- 3% for the clinical and dipyridamole-thallium models. Among the validation sets, areas were 74 +/- 9%, 72 +/- 7% and 76 +/- 5% for each center. Observed and estimated rates were comparable for both sets. By the clinical model, the observed rates were 3%, 8% and 18% for patients classified as low, moderate and high risk by clinical factors (p < 0.0001). The addition of dipyridamole-thallium data reclassified >80% of the moderate risk patients into low (3%) and high (19%) risk categories (p < 0.0001) but provided no stratification for patients classified as low or high risk according to the clinical model. Conclusions. Simple clinical markers, weighted according to prognostic impact, will reliably stratify risk in vascular surgery candidates referred for dipyridamole-thallium testing, thus obviating the need for the more expensive testing. Our prediction model retains its prognostic accuracy when applied to the validation sets and can reliably estimate risk in this group. C1 MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CAMBRIDGE,MA. UNIV MASSACHUSETTS,MED CTR,DEPT NUCL MED,WORCESTER,MA. UNIV MASSACHUSETTS,MED CTR,DEPT VASC SURG,WORCESTER,MA. NORTHWESTERN UNIV,DIV CARDIOL,CHICAGO,IL 60611. NORTHWESTERN UNIV,DIV CRIT CARE,CHICAGO,IL 60611. DEACONESS HOSP,DIV CARDIOVASC,BOSTON,MA. DEACONESS HOSP,INST PREVENT CARDIOVASC DIS,BOSTON,MA. JOHNS HOPKINS UNIV,DEPT ANESTHESIOL,BALTIMORE,MD. UNIV VERMONT,COLL MED,CARDIOL UNIT,BURLINGTON,VT. UNIV MICHIGAN,MED CTR,HEART CARE PROGRAM,ANN ARBOR,MI. RP LItalien, GJ (reprint author), MASSACHUSETTS GEN HOSP,VASC UNIT,DEPT SURG,WANG ACC 458,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 46 TC 121 Z9 125 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 15 PY 1996 VL 27 IS 4 BP 779 EP 786 DI 10.1016/0735-1097(95)00566-8 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA UA134 UT WOS:A1996UA13400004 PM 8613603 ER PT J AU Glatt, CR AF Glatt, CR TI Phantom illness: Shattering the myth of hypochondria - Cantor,C, Fallon,B SO LIBRARY JOURNAL LA English DT Book Review RP Glatt, CR (reprint author), VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 SN 0363-0277 J9 LIBR J JI Libr. J. PD MAR 15 PY 1996 VL 121 IS 5 BP 90 EP 90 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA TZ905 UT WOS:A1996TZ90500152 ER PT J AU Gut, IG Wood, PD Redmond, RW AF Gut, IG Wood, PD Redmond, RW TI Interaction of triplet photosensitizers with nucleotides and DNA in aqueous solution at room temperature SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID SINGLE-STRAND BREAKS; LASER PHOTOLYSIS; EXCITED-STATES; QUANTUM YIELDS; PHOTOCHEMISTRY; NUCLEOSIDES; COMPONENTS; THYMINE; POLYNUCLEOTIDES; PHOTOREACTIONS AB The study of triplet excited state behavior of nucleic acids and component mononucleotides is hampered by the very small yields produced by direct photolysis. We have used high energy triplet sensitizers to generate these species in high yield, thus facilitating the study of their photophysical and photochemical behavior. Acetone-sensitized triplet formation of all triplet state nucleotides allowed nucleotide triplet-triplet absorption spectra to be measured. Triplet-triplet absorption coefficients were determined using comparative actinometry. Self-quenching of the nucleotide triplet states was found to occur efficiently with rate constants, k(sq) > 10(7) M(-1) s(-1). The interaction of a variety of ketone triplet sensitizers with mononucleotides has been studied as a function of the relative energies of the sensitizer-nucleotide pair. In all cases, the triplet states of the sensitizers were efficiently quenched by the nucleotides, although different reaction mechanisms were observed depending on the reaction pair under study. Acetone, the sensitizer with the highest triplet energy, sensitized all triplet state nucleotides. Sensitizers with triplet energies, E(T) > 74 kcal mol(-1), sensitized TMP and those with E(T) < 74 kcal mol(-1) did not exhibit any triplet sensitization, although an efficient quenching reaction (k(q) > 10(8) M(-1) s(-1)) was observed. Where energy transfer did not take place, sensitizers were quenched by electron transfer from the purines. The quantum yield for this process was determined as 0.31 for GMP and 0.09 for AMP. In DNA, triplet energy transfer from the same sensitizers was probed by determining the relative efficiency of pyrimidine dimer formation in pBR322, an exclusively triplet-mediated reaction under sensitized conditions. Our results allow some conclusions to be drawn on tripler properties and intramolecular energy transfer in DNA. Base triplet energy levels appear to be lower in DNA than in the isolated mononucleotides. In any system where ketone triplet states are generated, electron transfer from a purine should be considered as a significant reaction pathway. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 53 TC 103 Z9 104 U1 3 U2 15 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD MAR 13 PY 1996 VL 118 IS 10 BP 2366 EP 2373 DI 10.1021/ja9519344 PG 8 WC Chemistry, Multidisciplinary SC Chemistry GA UA029 UT WOS:A1996UA02900008 ER PT J AU Bubley, GJ Xu, J Kupiec, N Sanders, D Foss, F OBrien, M Emi, Y Teicher, BA Patierno, SR AF Bubley, GJ Xu, J Kupiec, N Sanders, D Foss, F OBrien, M Emi, Y Teicher, BA Patierno, SR TI Effect of DNA conformation on cisplatin adduct formation SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE cisplatin; chromatin; arginine butyrate ID NUCLEAR MATRIX; CIS-DIAMMINEDICHLOROPLATINUM(II); CHROMATIN; INVITRO; BINDING; TRANS-DIAMMINEDICHLOROPLATINUM(II); REPLICATION; INHIBITION; SEQUENCE; LINKING AB The anticancer drug cis-diamminedichloroplatinum(II) (cisplatin) has been shown previously to form adducts preferentially within internucleosomal or linker DNA rather than to DNA within the nucleosome. To determine whether other ''open'' regions of chromatin have an increased affinity for cisplatin, adduct formation within specific chromatin domains was analyzed. There was a significant increase in cisplatin-DNA adduct formation for DNA associated with the nuclear matrix (NM) compared with other chromatin domains and total unfractionated DNA. In contrast, treatment of the same cells with trans-diamminedichloroplatinum(II) (transplatin) did not result in preferential adduct formation. These findings led to the hypothesis that it might be possible to alter DNA to make it a more favorable target for cisplatin. The effect of arginine butyrate on cisplatin-DNA adduct formation was analyzed in human cancer cells. The combination of arginine butyrate and cisplatin resulted in a concentration-responsive increase in cisplatin-DNA adduct formation in PC-3 cells and an overall increase in cisplatin-DNA adduct formation in three other human cancer cell lines. The same combination also resulted in a significant increase in drug-induced cytotoxicity at a low concentration of cisplatin. These results suggest that chromatin configuration can affect cisplatin adduct formation. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02215. GEORGE WASHINGTON UNIV,MED CTR,DEPT PHARMACOL,WASHINGTON,DC 20037. BOSTON UNIV,MED CTR,DIV ONCOL,BOSTON,MA 02118. DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP Bubley, GJ (reprint author), BETH ISRAEL HOSP,DIV HEMATOL ONCOL,330 BROOKLINE AVE,BOSTON,MA 02215, USA. FU NCI NIH HHS [R01-CA 50174, R29-CA51438] NR 27 TC 16 Z9 17 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAR 8 PY 1996 VL 51 IS 5 BP 717 EP 721 DI 10.1016/S0006-2952(95)02256-2 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TW991 UT WOS:A1996TW99100020 PM 8615910 ER PT J AU Meng, W Ma, J Ayata, C Hara, H Huang, PL Fishman, MC Moskowitz, MA AF Meng, W Ma, J Ayata, C Hara, H Huang, PL Fishman, MC Moskowitz, MA TI Acetylcholine dilates pial arterioles in endothelial and neuronal nitric oxide synthase knockout mice by nitric oxide-dependent mechanisms SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 171 EP 171 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28400170 ER PT J AU Lee, SL Wang, WW Joseph, PM Hales, C Fanburg, BL AF Lee, SL Wang, WW Joseph, PM Hales, C Fanburg, BL TI The antihyperplastic and antihypertrophic effects of heparin on 5-HT-induced mitogenesis. SO FASEB JOURNAL LA English DT Meeting Abstract C1 TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02111. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 247 EP 247 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28400248 ER PT J AU Yuan, F Dellian, M Ferrara, N Jain, RK AF Yuan, F Dellian, M Ferrara, N Jain, RK TI Anti-VEGF antibody treatment reduces tumor vascular permeability to macromolecules. SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. GENENTECH INC,S SAN FRANCISCO,CA 94080. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 322 EP 322 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28400324 ER PT J AU Swartz, MA Berk, DA Jain, RK AF Swartz, MA Berk, DA Jain, RK TI Lymphatic transport of macromolecules and particles: Experimental and theoretical characterization. SO FASEB JOURNAL LA English DT Meeting Abstract C1 MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI Swartz, Melody/B-7633-2009; Swartz, Melody/F-9563-2011 NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 323 EP 323 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28400322 ER PT J AU Breton, S Brown, D AF Breton, S Brown, D TI Microtubule involvement in localization of apical (clathrin) and basolateral (Na-K-ATPase) proteins in proximal tubules. SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 495 EP 495 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28400496 ER PT J AU Adrie, C Holzmann, A Hirani, WM Hurford, WE Zapol, WM AF Adrie, C Holzmann, A Hirani, WM Hurford, WE Zapol, WM TI Effects of intravenous zaprinast and inhaled nitric oxide (NO) on pulmonary hemodynamics and gas exchange in an ovine model of acute respiratory failure. SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 551 EP 551 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28400549 ER PT J AU Thompson, BT Garg, HG Hales, CA AF Thompson, BT Garg, HG Hales, CA TI Antiproliferative activity of heparin resides in its glycosaminoglycan component SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 605 EP 605 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28400605 ER PT J AU Bao, HF Ma, H Sun, J Kleyman, TR Eaton, DC Ling, BN AF Bao, HF Ma, H Sun, J Kleyman, TR Eaton, DC Ling, BN TI Inhibition of amiloride-sensitive Na channels by luminal ATP in A6 distal nephron cells. SO FASEB JOURNAL LA English DT Meeting Abstract C1 EMORY UNIV,DEPT MED,DIV RENAL,ATLANTA,GA 30322. EMORY UNIV,DEPT MED,CTR CELL & MOL SIGNAL,ATLANTA,GA 30322. VET AFFAIRS MED CTR,ATLANTA,GA 30322. UNIV PENN,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 789 EP 789 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28400790 ER PT J AU Williams, AW Boileau, TWM Clinton, SK Erdman, JW AF Williams, AW Boileau, TWM Clinton, SK Erdman, JW TI beta-Carotene-enriched bovine serum - A physiologic vehicle to deliver carotenoids to prostate cancer cells in culture. SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV ILLINOIS,DEPT FOOD SCI,DIV NUTR SCI,URBANA,IL 61801. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1389 EP 1389 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401389 ER PT J AU Clinton, SK Williams, AW Boileau, TW Zhou, JR Northey, D Teicher, B Erdman, JW AF Clinton, SK Williams, AW Boileau, TW Zhou, JR Northey, D Teicher, B Erdman, JW TI Tissue distribution of lycopene isomers in nude mice bearing implants of human prostate adenocarcinoma. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV ILLINOIS,DIV NUTR SCI,URBANA,IL 61801. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1392 EP 1392 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401391 ER PT J AU Chandrasekar, B Freeman, GL AF Chandrasekar, B Freeman, GL TI Induction of antioxidant enzyme gene expression in myocardium during reperfusion after a transient SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,CARDIOL SECT,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1582 EP 1582 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401581 ER PT J AU Freeman, GL Chandrasekar, B AF Freeman, GL Chandrasekar, B TI Changes in myocardial pro-inflammatory cytokine gene expression and protein levels after transient ischemia followed by reperfusion. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1583 EP 1583 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401584 ER PT J AU Scremin, OU Jenden, DJ AF Scremin, OU Jenden, DJ TI Cerebral cortex choline and acetylcholine changes induced by trauma SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PHYSIOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PHARMACOL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1621 EP 1621 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401623 ER PT J AU Booth, RA Scremin, OU Jenden, DJ AF Booth, RA Scremin, OU Jenden, DJ TI Cognitive and behavioral changes induced by unilateral cortical trauma SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PHYSIOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PHARMACOL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1622 EP 1622 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401621 ER PT J AU Tang, T Frenette, PS Hynes, RO Wagner, DD Mayadas, TN AF Tang, T Frenette, PS Hynes, RO Wagner, DD Mayadas, TN TI Cytokine-induced meningitis is dramatically attenuated in mice deficient in endothelial selectins SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. MIT,HHMI,BOSTON,MA 02139. MIT,CTR CANC RES,BOSTON,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1625 EP 1625 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401625 ER PT J AU Beaumier, L Castillo, LC Young, VR AF Beaumier, L Castillo, LC Young, VR TI Effect of a dietary arginine supplement on protein metabolism in healthy adult men SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1636 EP 1636 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401634 ER PT J AU Jain, K Porch, J Reilly, A Mazariegos, M Valdez, C Ziegle, T Smith, RJ Solomons, NW AF Jain, K Porch, J Reilly, A Mazariegos, M Valdez, C Ziegle, T Smith, RJ Solomons, NW TI Relationships among physical activity, body composition and plasma insulin-like growth factor-1 (IGF-1) concentrations in elderly guatemalan woman SO FASEB JOURNAL LA English DT Meeting Abstract C1 CTR STUDIES SENSORY IMPAIRMENT AGING & METAB,GUATEMALA CITY,GUATEMALA. EMORY UNIV,SCH MED,ATLANTA,GA. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1659 EP 1659 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401660 ER PT J AU Holzmann, A Bloch, KD Sanchez, LS Filippov, G Zapol, WM AF Holzmann, A Bloch, KD Sanchez, LS Filippov, G Zapol, WM TI Lipopolysaccharide (LPS)-challenge decreases responsiveness to inhaled nitric oxide (NO) and increases pulmonary cGMP-phosphodiesterase (PDE) SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIOVASC RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1769 EP 1769 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401768 ER PT J AU Fukumura, D Yuan, F Jain, RK AF Fukumura, D Yuan, F Jain, RK TI Role of nitric oxide in tumor microcirculation SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 1905 EP 1905 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28401904 ER PT J AU Korent, VA Conhaim, RL Harms, BA AF Korent, VA Conhaim, RL Harms, BA TI Molecular distribution of hetastarch in lung lymph of unanesthetized sheep SO FASEB JOURNAL LA English DT Meeting Abstract C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,DEPT SURG,MADISON,WI 53705. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 2033 EP 2033 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28402032 ER PT J AU Jones, R GashiLuci, L AF Jones, R GashiLuci, L TI Lung microvascular injury and remodeling: Paraquat-induced fibrosis and effects of breathing high oxygen. SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. UNIV PRISTINA,DEPT PATHOL,PRISHTINA,YUGOSLAVIA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 2055 EP 2055 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28402055 ER PT J AU Koyal, SN Marques, J Lee, EY Cooper, CB Tashkin, DP AF Koyal, SN Marques, J Lee, EY Cooper, CB Tashkin, DP TI Ventilatory threshold and arterial blood gases during max stress test in habitual and non-habitual female cocaine users. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 2170 EP 2170 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28402170 ER PT J AU McCarthy, KM Skare, IB Stankewich, MC Furuse, M Tsukita, S Rogers, RA Lynch, RD Schneeberger, EE AF McCarthy, KM Skare, IB Stankewich, MC Furuse, M Tsukita, S Rogers, RA Lynch, RD Schneeberger, EE TI Occludin is a functional component of the tight junction. SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV MASSACHUSETTS,LOWELL,MA 01854. KYOTO UNIV,KYOTO,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 2320 EP 2320 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28402321 ER PT J AU Joseph, A Jueppner, H Gwosdow, A AF Joseph, A Jueppner, H Gwosdow, A TI Identification of the intracellular portion responsible for interleukin-1 activation of protein kinase A SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 2437 EP 2437 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28402436 ER PT J AU Zhou, JR Blackburn, GL Clinton, SK AF Zhou, JR Blackburn, GL Clinton, SK TI Soy derived isoflavones in combination with interferon gamma (INF gamma) inhibit proliferation of bladder carcinoma cells in vitro. SO FASEB JOURNAL LA English DT Meeting Abstract C1 NEW ENGLAND DEACONESS HOSP,DEPT NUTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 2867 EP 2867 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28402865 ER PT J AU Thomas, A Rao, S Haung, P Fishman, MC Prabhakar, NR AF Thomas, A Rao, S Haung, P Fishman, MC Prabhakar, NR TI Blunted ventilatory response to hypoxia in mice with disrupted neuronal nitric oxide synthase (nNOS) gene. SO FASEB JOURNAL LA English DT Meeting Abstract C1 CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 3673 EP 3673 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28403672 ER PT J AU Hoop, B Johnson, DC Kazemi, H Peng, CK Goldberger, AL AF Hoop, B Johnson, DC Kazemi, H Peng, CK Goldberger, AL TI Long-range correlation in phrenic neural noise SO FASEB JOURNAL LA English DT Meeting Abstract C1 BETH ISRAEL HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RI Peng, Chung-Kang/E-1489-2011 OI Peng, Chung-Kang/0000-0003-3666-9833 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 3711 EP 3711 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28403711 ER PT J AU Du, HK Thompson, DT Garg, HG Hales, CA AF Du, HK Thompson, DT Garg, HG Hales, CA TI Effects of dimethyl amiloride (DMA) on hypoxic pulmonary hypertension in rats. SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 3728 EP 3728 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28403728 ER PT J AU Evans, AB Tsai, LW Oelberg, D Beagle, J Systrom, DM AF Evans, AB Tsai, LW Oelberg, D Beagle, J Systrom, DM TI Compartmentation of arterial, skeletal muscle ECF, and ICF pH regulation during exercise in rat. SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULMON & CRIT CARE UNIT,BOSTON,MA. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,NMR LAB PHYSIOL CHEM,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 3858 EP 3858 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28403856 ER PT J AU Rajavashisth, TB Bergner, EA Clinton, SK Lee, WNP AF Rajavashisth, TB Bergner, EA Clinton, SK Lee, WNP TI Dietary fat intake does not affect cholesterol recycling in low density lipoprotein receptor-deficient mice. SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,HARBOR MED CTR,TORRANCE,CA 90509. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 4175 EP 4175 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28404173 ER PT J AU Thorin, E Huang, P Fishman, MC Bevan, JA AF Thorin, E Huang, P Fishman, MC Bevan, JA TI alpha(2)-Adrenoceptor stimulation induces vasodilation in mice lacking the gene for endothelial nitric oxide synthase SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV VERMONT,DEPT PHARMACOL,BURLINGTON,VT 05405. HARVARD UNIV,SCH MED,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 8 PY 1996 VL 10 IS 3 BP 4672 EP 4672 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA TZ284 UT WOS:A1996TZ28404672 ER PT J AU Puri, KD Springer, TA AF Puri, KD Springer, TA TI A Schiff base with mildly oxidized carbohydrate ligands stabilizes L-selectin and not P-selectin or E-selectin rolling adhesions in shear flow SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NODE HOMING RECEPTOR; FUNCTIONAL-CHARACTERIZATION; VASCULAR ADDRESSIN; CELL-ADHESION; SIALIC ACIDS; RECOGNITION; BINDING; IDENTIFICATION; NEUTROPHILS; LEUKOCYTES AB Selectins are a family of lectins, that mediate tethering and rolling of leukocytes on endothelium in vascular shear flow. Mild periodate oxidation of the L-selectin ligand CD34, or L-selectin ligands on leukocytes, enhanced resistance to detachment in shear and decreased rolling velocity equivalent to an 8-fold increase in ligand density, yet had little effect on the rate of tethering, Enhanced interactions were also seen with mildly oxidized sialyl Lewis(a) and sialyl Lewis(x) glycolipids, Enhancement was completely reversed by borohydride reduction, yielding a strength of interaction equivalent to that with the native ligands. No effect on the strength of P-selectin and E-selectin interactions was seen after mild oxidation of their ligands, Completeness of modification of sialic acid by mild periodate was verified with monoclonal antibody to sialyl Lewis(x)-related structures and resistance to neuraminidase, The addition of cyanoborohydride to leukocytes rolling through L-selectin on mildly oxidized but not native CD34 caused arrest of rolling cells and formation of EDTA-resistant bonds to the substrate, suggesting that a Schiff base was reduced, Cyanoborohydride reduction of mildly oxidized cells rolling on P-selectin and E-selectin also caused arrest and formation of EDTA-resistant bonds but with slower kinetics, These data suggest that interactions with a sialic acid aldehyde group on mildly oxidized ligands that include interconversion to a Schiff base can occur with three selectins yet only stabilize binding through the selectin with the fastest k(off), L-selectin. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,CTR BLOOD RES,BOSTON,MA 02115. FU NCI NIH HHS [CA31799]; NHLBI NIH HHS [HL48675] NR 45 TC 19 Z9 19 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 8 PY 1996 VL 271 IS 10 BP 5404 EP 5413 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TZ286 UT WOS:A1996TZ28600021 PM 8621395 ER PT J AU Paoli, M Liddington, R Tame, J Wilkinson, A Dodson, G AF Paoli, M Liddington, R Tame, J Wilkinson, A Dodson, G TI Crystal structure of T state haemoglobin with oxygen bound at all four haems SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE haemoglobin; cooperativity; T state; oxygenation; crystallography ID HUMAN-HEMOGLOBIN; BINDING; DEOXYHEMOGLOBIN; RESOLUTION AB The cooperative binding of oxygen by haemoglobin results from restraints on ligand binding in the T state. The unfavourable interactions made by the ligands at the haems destabilise the T state and favour the high affinity R state. The T double left right arrow R equilibrium leads, in the presence of a ligand, to a rapid increase in the R state population and therefore generates cooperative binding. There is now considerable understanding of this phenomenon, but the interactions that reduce ligand affinity in the T state have not yet been fully explored, owing to the difficulties in preparing T state haemoglobin crystals in which all the subunits are oxygenated. A protocol has been developed to oxygenate deoxy T state adult human haemoglobin (HbA) crystals in air at 4 degrees C at all four haems without significant loss of crystalline order. The X-ray crystal structure, determined to 2.1 Angstrom spacing, shows significant changes in the alpha and beta haem pockets as well as changes at the alpha(1) beta(2) interface in the direction of the R quaternary structure. Most of the shifts and deviations from deoxy T state HbA are similar to, but larger than, those previously observed in the T state met and other partially liganded T state forms. They provide clear evidence of haem-haem interaction in the T state. (C) 1996 Academic Press Limited C1 DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NATL INST MED RES,LONDON NW7 1AA,ENGLAND. RP Paoli, M (reprint author), UNIV YORK,DEPT CHEM,YORK YO1 5DD,N YORKSHIRE,ENGLAND. OI Wilkinson, Anthony/0000-0003-4577-9479 NR 27 TC 107 Z9 110 U1 4 U2 24 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD MAR 8 PY 1996 VL 256 IS 4 BP 775 EP 792 DI 10.1006/jmbi.1996.0124 PG 18 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TX629 UT WOS:A1996TX62900010 PM 8642597 ER PT J AU Saling, P Carballada, R Burks, D Moore, H AF Saling, P Carballada, R Burks, D Moore, H TI Sperm-egg binding protein or proto-oncogene? Reply SO SCIENCE LA English DT Article ID EVOLUTION C1 DUKE UNIV,MED CTR,DEPT CELL BIOL,DURHAM,NC 27710. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02215. UNIV SHEFFIELD,DEPT MOLEC BIOL & BIOTECHNOL,SHEFFIELD S10 2UH,S YORKSHIRE,ENGLAND. RP Saling, P (reprint author), DUKE UNIV,MED CTR,DEPT OBSTET & GYNECOL,DURHAM,NC 27710, USA. NR 11 TC 2 Z9 2 U1 0 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 8 PY 1996 VL 271 IS 5254 BP 1434 EP 1435 DI 10.1126/science.271.5254.1434 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TY961 UT WOS:A1996TY96100052 PM 17814026 ER PT J AU Verheij, M Bose, R Lin, XH Yao, B Jarvis, WD Grant, S Birrer, MJ Szabo, E Zon, LI Kyriakis, JM HaimovitzFriedman, A Fuks, Z Kolesnick, RN AF Verheij, M Bose, R Lin, XH Yao, B Jarvis, WD Grant, S Birrer, MJ Szabo, E Zon, LI Kyriakis, JM HaimovitzFriedman, A Fuks, Z Kolesnick, RN TI Requirement for ceramide-initiated SAPK/JNK signalling in stress-induced apoptosis SO NATURE LA English DT Article ID KINASE; DEATH AB The induction of programmed cell death, or apoptosis, involves activation of a signalling system, many elements of which remain unknown(1). The sphingomyelin pathway, initiated by hydrolysis of the phospholipid sphingomyelin in the cell membrane to generate the second messenger ceramide(2,3), is thought to mediate apoptosis in response to tumour-necrosis factor (TNF)-alpha(2,3), to Fas ligand(4) and to X-rays(5). It is not known whether it plays a role in the stimulation of other forms of stress-induced apoptosis. Given that environmental stresses also stimulate a stress-activated protein kinase (SAPR/JNK)(6-12), the sphingomyelin and SAPK/ JNK signalling systems may be coordinated in induction of apoptosis. Here we report that ceramide initiates apoptosis through the SAPK cascade and provide evidence for a signalling mechanism that integrates cytokine- and stress-activated apoptosis. C1 MEM SLOAN KETTERING CANC CTR,LAB SIGNAL TRANSDUCT,NEW YORK,NY 10021. MEM SLOAN KETTERING CANC CTR,DEPT RADIAT ONCOL,NEW YORK,NY 10021. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MED,DIV HEMATOL ONCOL,RICHMOND,VA 23298. NCI,DIV CANC PREVENT & CONTROL,BIOMARKERS & PREVENT RES BRANCH,ROCKVILLE,MD 20850. CHILDRENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT PEDIAT,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT PEDIAT,DANA FARBER CANC INST,CHILDRENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP EAST,MED SERV,DIABET RES LAB,BOSTON,MA 02129. NR 30 TC 1632 Z9 1671 U1 3 U2 47 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD MAR 7 PY 1996 VL 380 IS 6569 BP 75 EP 79 DI 10.1038/380075a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TY877 UT WOS:A1996TY87700060 PM 8598911 ER PT J AU Hsu, HB Yu, YM Babich, JW Burke, JF Livni, E Tompkins, RG Young, VR Alpert, NM Fischman, AJ AF Hsu, HB Yu, YM Babich, JW Burke, JF Livni, E Tompkins, RG Young, VR Alpert, NM Fischman, AJ TI Measurement of muscle protein synthesis by positron emission tomography with L-[methyl-C-11]methionine SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE hind limb; arterio-venous difference; stable isotope; paraspinal muscle; dog ID LEUCINE METABOLISM; SYNTHESIS RATES; AMINO-ACIDS; KINETICS; INVIVO; HUMANS; MODEL; PET; INJURY AB Positron emission tomography (PET) with L-[methyl-C-11]methionine was explored as an in vivo, noninvasive, quantitative method for measuring the protein synthesis rate (PSR) in paraspinal and hind limb muscles of anesthetized dogs. Approximately 25 mCi (1 Ci = 37 GBq) of L-[methyl-C-11]methionine was injected intravenously, and serial images and arterial blood samples were acquired over 90 min. Data analysis was performed by fitting tissue- and metabolite-corrected arterial blood time-activity curves to a three-compartment model and assuming insignificant transamination and transmethylation in this tissue. PSR was calculated from fitted parameter values and plasma methionine concentrations. PSRs measured by PET were compared with arterio-venous (A-V) difference measurements across the hind limb during primed constant infusion (5-6 h) of L-[1-C-13, methyl-H-2(3)]methionine. Results of PET measurements demonstrated similar PSRs for paraspinal and hind limb muscles: 0.172 +/- 0.062 vs. 0.208 +/- 0.048 nmol(-1). min(-1).(g of muscle)(-1) (P = not significant). PSR determined by the stable isotope technique was 0.27 +/- 0.050 nmol(-1). min(-1).(g of leg tissue)(-1) (P < 0.07 from PET) and indicated that the contribution of transmethylation to total hind limb methionine utilization was approximate to 10%. High levels of L-[methyl-C-11] methionine utilization by bone marrow were observed. We conclude that muscle PSR can be measured in vivo by PET and that this approach offers promise for application in human metabolic studies. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,TRAUMA SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. SHRINERS BURNS INST,BOSTON,MA. FU NCI NIH HHS [T32-CA09302]; NIGMS NIH HHS [T32-GM07035, P50-GM21700] NR 37 TC 14 Z9 14 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 5 PY 1996 VL 93 IS 5 BP 1841 EP 1846 DI 10.1073/pnas.93.5.1841 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TY964 UT WOS:A1996TY96400020 PM 8700846 ER PT J AU Xu, Y Davidson, L Alt, FW Baltimore, D AF Xu, Y Davidson, L Alt, FW Baltimore, D TI Function of the pre-T-cell receptor alpha chain in T-cell development and allelic exclusion at the T-cell receptor beta locus SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE gene targeting; T-cell differentiation; allelic exclusion ID TRANSGENIC MICE; TARGETED DISRUPTION; IMMUNOGLOBULIN-MU; MEMBRANE EXON; GENES; EXPRESSION; ANTIGEN; MUTATIONS; PROTEIN; RAG-2 AB The pre-T-cell receptor, composed of the T-cell receptor (TCR) beta chain (TCR beta), pre-T alpha (pT alpha) chain, and CD3 molecules, has been postulated to be a transducer of signals during the early stages of T-cell development, To examine the function of the transmembrane pT alpha chain during thymocyte development, we generated pT alpha(-/-) embryonic stem cells and assayed their ability to differentiate Into lymphoid cells in vivo after injection into recombination-activating gene (RAG)-2-deficient blastocysts, Thymocytes representing all stages of T-cell differentiation were detected In the thymus of pT alpha(-/-) chimeric mice, indicating that thymocyte development can occur without pT alpha. However, greatly reduced thymocyte numbers and substantially increased percentages of both CD4(-)CD8(-) thymocytes and TCR gamma delta(+) thymocytes suggest that pT alpha plays a critical role in thymocyte expansion, To investigate the role of the pT alpha chain in allelic exclusion at the TCR beta locus, a functionally rearranged TCR beta minigene was introduced into pT alpha(-/-) and pT alpha(+/-) embryonic stem cells, which were subsequently assayed by RAG-2-deficient blastocyst complementation. In the absence of pT alpha, expression of the transgenic TCR beta inhibited rearrangement of the endogenous TCR beta locus to an extent similar to that seen in normal TCR beta transgenic mice, suggesting that pT alpha may not be required for signaling allelic exclusion at the TCR beta locus. C1 CHILDRENS HOSP,DEPT GENET & PEDIAT,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RP Xu, Y (reprint author), MIT,DEPT BIOL,CAMBRIDGE,MA 02139, USA. NR 29 TC 58 Z9 59 U1 1 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 5 PY 1996 VL 93 IS 5 BP 2169 EP 2173 DI 10.1073/pnas.93.5.2169 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TY964 UT WOS:A1996TY96400080 PM 8700903 ER PT J AU Barnhart, J Shekelle, P Lewis, C AF Barnhart, J Shekelle, P Lewis, C TI The effect of a medical school's admission and curriculum policies on increasing the number physicians in primary care specialties SO ACADEMIC MEDICINE LA English DT Article AB Purpose. The Charles R. Drew University of Medicine and Science, which is affiliated with the University of California, Los Angeles, UCLA School of Medicine, has a mission to increase the number of physicians pursuing careers in primary care and/or providing care to the underserved. The authors sought to determine whether Drew's initial classes are pursuing career paths consistent with the institution's mission. Method. In June 1992 the alumni from the Drew and UCLA classes of 1985 through 1987 were mailed questionnaires to ascertain their specialty choices and practice settings. Responses were analyzed using bivariate analyses and multiple logistic regression. Results. The response rates were 89% (402 of 454) for the UCLA graduates and 76% (44 of 58) for the Drew graduates. Bivariate analyses showed that Hispanics, women, older individuals, and Drew graduates were more likely ro choose primary care specialties (p < .001 for each variable). Multiple logistic regression also showed that these variables predicted primary care career choice: for being a Hispanic, odds ratio (OR) = 3.2, 95% CI (1.66, 6.35); for being a woman, OR = 1.9, 95% CI (1.28, 2.97); for being older, OR = .92, 95% CI (.86, .99); and for being a Drew graduate, OR = 2.4, 95% CI (1.09, 5.27). Older graduates practiced in underserved areas more than did younger ones (26% vs 13%, p = .03). Conclusion. To some degree, Drew has fulfilled its mission of graduating physicians who are primary care specialists and/or practice in underserved areas; however, the results raise questions regarding possible early influences on career choice. C1 YESHIVA UNIV,ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY 10461. UNIV CALIF LOS ANGELES,DIV GEN INTERNAL MED & HLTH SERV RES,LOS ANGELES,CA. W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,CTR HLTH PROMOT & DIS PREVENT,LOS ANGELES,CA. VET AFFAIRS HLTH SERV,RES & DEV SERV,LOS ANGELES,CA. RP Barnhart, J (reprint author), YESHIVA UNIV,ALBERT EINSTEIN COLL MED,DEPT EPIDEMIOL & SOCIAL MED,BELFER 1306A,BRONX,NY 10461, USA. FU BHP HRSA HHS [2-T32-PE-19001-06] NR 9 TC 7 Z9 7 U1 0 U2 1 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1040-2446 J9 ACAD MED JI Acad. Med. PD MAR PY 1996 VL 71 IS 3 BP 293 EP 295 DI 10.1097/00001888-199603000-00025 PG 3 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA UA032 UT WOS:A1996UA03200030 PM 8607932 ER PT J AU Goldberg, SN Gazelle, GS Halpern, EF Rittman, WJ Mueller, PR Rosenthal, DI AF Goldberg, SN Gazelle, GS Halpern, EF Rittman, WJ Mueller, PR Rosenthal, DI TI Radiofrequency tissue ablation: Importance of local temperature along the electrode tip exposure in determining lesion shape and size SO ACADEMIC RADIOLOGY LA English DT Article DE radiofrequency; tissue ablation; lesion; tissue coagulation AB Rationale and Objectives. We determined whether heat distribution along a radiofrequency (RF) electrode would be uniform when longer tip exposures are used and whether local temperature effects would influence the shape of induced tissue coagulation. Methods. Thermistors were embedded within 18-gauge RF electrodes at both ends and in the middle of the exposed tip, The length of tip exposure p varied from 1 to 7 cm, RF was applied in vitro to pig liver for G rlin using a constant tip temperature, which was varied in 10 degrees C increments from 60 degrees C to 110 degrees C. Experiments were performed in triplicate, The 3- and 5-cm probes were used at a 30 degrees C tip temperature to create lesions in live pig liver and muscle using similar parameters. Temperature was measured throughout the procedure. Observable coagulation necrosis was measured at the end of the treatment, Regression analysis was used to evaluate the local temperature-lesion diameter relationship. Results. Temperatures were not uniform along the tip exposure for any given trial, Temperature variation increased with higher tip temperatures and longer tip exposures. The diameter of local coagulation necrosis was a function of the local mean temperature. For in vitro trials, no coagulation was seen when the local temperature was less than 50 degrees C. Temperatures above this threshold resulted in progressively greater lesion diameter, with a minimum of 1 cm Of necrosis occurring at 71 degrees C. Additional increases in lesion diameter (1.4-1.6 cm) were observed at approximately 90 degrees C. Mathematical modeling demonstrated a best-fit curve: lesion diameter (in cm) = (1.4 + 0.03 (tip exposure)] {1 - e([-0.067(local temp - 49.5 degrees C)])}, r(2) = .986, SD = 0.14 cm for each curve. In living tissue, less uniformity in the shape of coagulation necrosis was seen around the electrodes, Local temperature-lesion diameter data fit the same logarithmic relation, but the threshold for coagulation necrosis was 8.5 degrees C higher than for in vitro specimens. Conclusion. Using a single-probe technique for RF-induced tissue necrosis, the diameter of tissue coagulation may be predicted by the local temperature along tile exposed electrode. The uniformity of temperature decreases with increased tip exposures. This effect may be partially corrected by creating lesions at higher tip temperatures, where necrosis diameter is increased, Because effects are more pronounced in vivo, uniform volumes of tissue necrosis are limited to tip exposures of 3 cm or less. C1 RADIONICS INC,BURLINGTON,MA. RP Goldberg, SN (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 11 TC 182 Z9 194 U1 1 U2 8 PU ASSOC UNIV RADIOLOGISTS PI RESTON PA 1891 PRESTON WHITE DR, RESTON, VA 22091 SN 1076-6332 J9 ACAD RADIOL JI Acad. Radiol. PD MAR PY 1996 VL 3 IS 3 BP 212 EP 218 DI 10.1016/S1076-6332(96)80443-0 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TY101 UT WOS:A1996TY10100006 PM 8796667 ER PT J AU Trubetskoy, VS FrankKamenetsky, MD Whiteman, KR Wolf, GL Torchilin, VP AF Trubetskoy, VS FrankKamenetsky, MD Whiteman, KR Wolf, GL Torchilin, VP TI Stable polymeric micelles: Lymphangiographic contrast media for gamma scintigraphy and magnetic resonance imaging SO ACADEMIC RADIOLOGY LA English DT Article DE micelles; polyoxyethylene; lymphography; scintigraphy; magnetic resonance imaging ID AGENT; LYMPHOSCINTIGRAPHY; LIPOSOMES; RABBITS AB Rationale and Objectives. Amphiphilic biocompatible polyoxyethylene (PEO)-based polymers form particles (micelles) that are 10-50 nm in diameter. In the current research, we successfully incorporated amphiphilic indium-111 (In-111) and gadolinium chelates into these particles and used them as particulate contrast media in percutaneous lymphography. Methods. Micelles of amphiphilic PEG-lipid conjugates were loaded with In-111 and gadolinium diethylenetriamine pentaacetic acid-phosphatidylethanolamine (Gd-DTPA-PE) and were injected subcutaneously into the rabbit's paw. Corresponding images of local lymphatics were acquired using a gamma camera and a magnetic resonance (MR) imager. Results. The entire lymphatic chain from the paw to the thoracic duct could be visualized using In-111 micelles after injection site massage. T1-weighted MR images of the primary lymph node and collecting vessels were obtained within 4 min after administration of gadolinium micelles and massage. Era Conclusion. Polymeric PEG-containing micelles can be loaded with diagnostic metals and, on subcutaneous injection, can visualize elements of lymphatic system. The major fraction of injected micelles stays within the lymph fluid, thus serving as lymphangiographic agents for indirect MR or gamma lymphography. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP Trubetskoy, VS (reprint author), MASSACHUSETTS GEN HOSP EAST,CTR IMAGING & PHARMACEUT RES,149 13TH ST,BOSTON,MA 02129, USA. NR 30 TC 40 Z9 43 U1 0 U2 7 PU ASSOC UNIV RADIOLOGISTS PI RESTON PA 1891 PRESTON WHITE DR, RESTON, VA 22091 SN 1076-6332 J9 ACAD RADIOL JI Acad. Radiol. PD MAR PY 1996 VL 3 IS 3 BP 232 EP 238 DI 10.1016/S1076-6332(96)80448-X PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TY101 UT WOS:A1996TY10100009 PM 8796670 ER PT J AU Centeno, BA Kuebler, D Warshaw, AL Lewandrowski, KB AF Centeno, BA Kuebler, D Warshaw, AL Lewandrowski, KB TI Peritoneal fluid cytology in advanced mucinous cystadenocarcinoma of the pancreas SO ACTA CYTOLOGICA LA English DT Article DE peritoneal fluid; cystadenocarcinoma, mucinous; pancreatic neoplasms ID FREE CANCER-CELLS; CARCINOMA; DISEASE AB OBJECTIVE: To assess the role of peritoneal cytology in the management of mucinous cystadenocarcinoma. STUDY DESIGN: A review of the peritoneal fluid cytologic findings in eight selected cases of pancreatic mucinous cystadenocarcinomas. RESULTS: Four of eight cases (50%) were positive for malignant cells. All four patients with positive peritoneal cytology had unresectable tumors and extensive intraabdominal metastases. Of the Jour patients with negative cytology, three had unresectable, locally invasive tumors without metastases, and one had a resectable turner confined to the pancreas. CONCLUSION: Peritoneal cytology is frequently positive in unresectable mucinous cystadenocarcinomas with intraabdominal metastases, but cytology may often be negative in unresectable cases. Therefore, negative cytologic findings in these cases do not reliably ensure resectability, while positive findings clearly correlate with the presence of intraabdominal metastases. A larger study of unselected patients, including more with resectable tumors, will be required to define the full utility of this technique in preoperative assessment. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. NR 14 TC 2 Z9 2 U1 0 U2 0 PU SCI PRINTERS & PUBL INC PI ST LOUIS PA P.O. DRAWER 12425 8342 OLIVE BLVD, ST LOUIS, MO 63132 SN 0001-5547 J9 ACTA CYTOL JI Acta Cytol. PD MAR-APR PY 1996 VL 40 IS 2 BP 191 EP 195 PG 5 WC Pathology SC Pathology GA UD400 UT WOS:A1996UD40000007 PM 8629396 ER PT J AU Paulus, W Lisle, DK Tonn, JC Wolf, HK Roggendorf, W Reeves, SA Louis, DN AF Paulus, W Lisle, DK Tonn, JC Wolf, HK Roggendorf, W Reeves, SA Louis, DN TI Molecular genetic alterations in pleomorphic xanthoastrocytoma SO ACTA NEUROPATHOLOGICA LA English DT Article DE astrocytoma; epidermal growth factor receptor; glioma p53; loss of heterozygosity ID EPIDERMAL GROWTH-FACTOR; BRAIN-TUMOR SPECIMENS; FACTOR RECEPTOR; CLASSIFICATION; AMPLIFICATION; MUTATIONS; FEATURES; GLIOMAS; TISSUE AB Pleomorphic xanthoastrocytoma (PXA) is a low-grade glioma that may recur as a malignant diffuse astrocytoma such as glioblastoma (GEM). While the molecular genetic basis of diffuse astrocytomas has been studied extensively, PXAs have not been analyzed in detail. We, therefore analyzed DNA from archival primary and recurrent PXAs from eight patients (three grade II PXAs without recurrence, one grade II PXA with recurrence as grade Il PXA, two grade II PXAs with progression to GEM, and two grade III anaplastic PXAs with recurrence as grade III anaplastic PXA or GEM) for genetic changes associated with diffuse astrocytomas. Single-strand conformation polymorphism analysis of p53 exons 5-8 revealed migration shifts in two cases, one primary PXA without recurrence and one recurrent grade II PXA in which the primary tumor did not show a shift. DNA sequencing showed two missense mutations in codons 220 (exon 6) and 292 (exon 8), respectively, mutations which have not been previously noted in astrocytomas. Differential polymerase chain reaction analysis demonstrated epidermal growth factor receptor gene amplification in only one tumor, a GEM without allelic loss of chromosome 10 that was the second GEM recurrence of an initial grade II PXA. Loss of heterozygosity studies on tumors from five patients, using three microsatellite polymorphisms on chromosome 10q and three on chromosome 19q, did not disclose allelic loss in any recurrent tumor. These findings suggest that the genetic events that underlie PXA formation and progression may differ significantly from those involved in diffuse astrocytoma tumorigenesis. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. UNIV WURZBURG,DEPT NEUROSURG,W-8700 WURZBURG,GERMANY. UNIV BONN,INST NEUROPATHOL,W-5300 BONN,GERMANY. UNIV WURZBURG,INST PATHOL NEUROPATHOL,W-8700 WURZBURG,GERMANY. RP Paulus, W (reprint author), UNIV ZURICH HOSP,INST NEUROPATHOL,SCHMELZBERGSTR 12,CH-8091 ZURICH,SWITZERLAND. FU NCI NIH HHS [CA 57683] NR 29 TC 44 Z9 46 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0001-6322 J9 ACTA NEUROPATHOL JI Acta Neuropathol. PD MAR PY 1996 VL 91 IS 3 BP 293 EP 297 PG 5 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA TV293 UT WOS:A1996TV29300010 PM 8834542 ER PT J AU Goetz, MB AF Goetz, MB TI Relationship between fluconazole dosage regimens and the emergence of fluconazole-resistant Candida albicans SO AIDS LA English DT Editorial Material DE fluconazole; Candida albicans; candidiasis ID AIDS; INDIVIDUALS; STRAINS; TRENDS C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. RP Goetz, MB (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,INFECT DIS SECT,DEPT MED,112F,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. OI Goetz, Matthew/0000-0003-4542-992X NR 18 TC 6 Z9 6 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD MAR PY 1996 VL 10 IS 3 BP 335 EP 336 DI 10.1097/00002030-199603000-00013 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA UB187 UT WOS:A1996UB18700013 PM 8882674 ER PT J AU Premkumar, DRD Ma, XZ Maitra, RK Chakrabarti, BK Salkowitz, J YenLieberman, B Hirsch, MS Kestler, HW AF Premkumar, DRD Ma, XZ Maitra, RK Chakrabarti, BK Salkowitz, J YenLieberman, B Hirsch, MS Kestler, HW TI The nef gene from a long-term HIV type 1 nonprogressor SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; CYTOTOXIC T-LYMPHOCYTES; PROTEIN; INVIVO; CELLS; REPLICATION; SEQUENCES; INDUCTION; DISEASE; INVITRO AB We examined the nef gene of HIV-I in a long-term nonprogressor to look for evidence suggesting an attenuated virus. The nef gene was previously shown to be required for induction of AIDS, Simian immunodeficiency virus (SIV) deleted in nef, while infectious, fails to sustain the high viral loads necessary for the induction of AIDS in infected adult rhesus monkeys, The human subject of this report was found to harbor virus (HIV-1 Sur25) encoding open-nef reading frames, However, the nef genes of this subject bore a signature point mutation: a cysteine at amino acid 138, The sequence at this position was identical in all clones examined over a 3-year period, When this sequence was compared to the sequence database for AIDS and human retroviruses at Los Alamos, New Mexico several isolates from other asymptomatic individuals were also found to encode nef genes with a cysteine at position 138. Furthermore, Cys-138 was found in chimpanzee immunodeficiency virus (CIV), a lentivirus that is similar to HIV but does not cause AIDS in chimpanzees, Multiple cysteines are also found in the nef gene of African green monkey virus, SVIagm, including cysteine at the position analogous to Cys-138. While seroprevalence of SIVagm is high in the wild, there is no known disease associated with this virus, The pathogenic virus isolated from Asian macaques, SIVmac, encodes a Nef protein that has few cysteines, Although the virus HIVSur25 encodes a completely open-nef gene, the virus from this individual is similar to attenuated SIVmac (SIVmac239/nef-deletion) as well as HIV deleted in nef in its growth properties in H9 cells. Nef containing a cysteine at position 138 was shown to be responsible for determining the ability to grow in H9. C1 CLEVELAND CLIN FDN,DEPT LAB MED,CLEVELAND,OH 44195. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,CAMBRIDGE,MA 02114. RI chakrabarti, bikas/F-4825-2013 FU NCI NIH HHS [CA12434] NR 46 TC 39 Z9 39 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAR 1 PY 1996 VL 12 IS 4 BP 337 EP 345 DI 10.1089/aid.1996.12.337 PG 9 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA UD140 UT WOS:A1996UD14000010 PM 8906995 ER PT J AU Gonzalez, RG Guimaraes, AR Moore, GJ Crawley, A Cupples, LA Growdon, JH AF Gonzalez, RG Guimaraes, AR Moore, GJ Crawley, A Cupples, LA Growdon, JH TI Quantitative in vivo P-31 magnetic resonance spectroscopy of Alzheimer disease SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article DE Alzheimer disease; magnetic resonance spectroscopy; high-energy phosphates; phospholipid metabolism ID POSITRON EMISSION TOMOGRAPHY; ENERGY-METABOLISM; NMR-SPECTROSCOPY; SENILE DEMENTIA; BRAIN; DIAGNOSIS; INVIVO; QUANTIFICATION; PATHOGENESIS; INVITRO AB The purpose of this study was to determine whether, in Alzheimer disease (AD) patients, abnormalities in energy charge or phospholipid metabolism could be detected during life with quantitative phosphorus magnetic resonance spectroscopy (P-31 MRS). We performed in vivo P-31 MRS in 16 patients with a clinical diagnosis of probable AD with mild to moderate dementia severity (mean Blessed Dementia Score = 17.5, range = 7-37) and in 8 healthy, nondemented, age-matched, control subjects. MR studies were performed on a commercial 1.5 T MR imager using a volume head coil. We acquired brain spectra by sampling a 6-cm-thick axial slice through the cerebrum (a region that includes similar to 900 ml of brain tissue); we measured beta-nucleoside triphosphate (beta-NTP), phosphocreatine (PCr), phosphomonoesters (PME), phosphodiesters (PDE), and inorganic phosphate (P-i) concentrations, then calculated ratios of these resonances. The beta-NTP, PCr, and P-i resonances in AD and control subjects were not significantly different. These data indicate that brain energy stores are not depleted in AD. No significant differences were detected in the absolute measurements of PME and PDE between the AD and control groups. However, among the calculated ratios, an increase in the PME/PDE ratio of similar to 50%, mostly due to a decrease in the PDE signal, was statistically significant (AD PME/PDE mean = 0.35, range 0.13-0.71; normal PME/PDE mean = 0.22, range 0.16-0.34). We speculate that the difference in PDE reflects changes in the biophysical state of membrane phospholipids in AD. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,SCH PUBL HLTH,BOSTON,MA. BOSTON UNIV,BOSTON,MA 02215. MIT,RADIOL SCI PROGRAM,CAMBRIDGE,MA 02139. RP Gonzalez, RG (reprint author), MASSACHUSETTS GEN HOSP,NMR CTR,13TH ST,BOSTON,MA 02129, USA. RI Moore, Gregory/E-7184-2010 OI Moore, Gregory/0000-0001-8541-3194 FU NIA NIH HHS [AG 10679, P50 AG 05134] NR 38 TC 23 Z9 24 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PD SPR PY 1996 VL 10 IS 1 BP 46 EP 52 DI 10.1097/00002093-199601010-00008 PG 7 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA TZ003 UT WOS:A1996TZ00300008 PM 8919496 ER PT J AU Smith, AJC Holt, RE Fitzpatrick, K Palacios, IF Gold, HK Werner, W Bovill, EG Fuster, V Jang, IK AF Smith, AJC Holt, RE Fitzpatrick, K Palacios, IF Gold, HK Werner, W Bovill, EG Fuster, V Jang, IK TI Transient thrombotic state after abrupt discontinuation of heparin in percutaneous coronary angioplasty SO AMERICAN HEART JOURNAL LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; UNSTABLE ANGINA-PECTORIS; FIBRINOPEPTIDE-A; COAGULATION; ACTIVATION; INSIGHTS; PLASMA AB Clinical and biochemical evidence of a rebound phenomenon after discontinuing thrombin inhibitors has been reported in patients with unstable angina. To investigate if a similar phenomenon occurs in patients undergoing coronary angioplasty, 14 patients were prospectively studied during and after discontinuation of heparin infusion. A transient thrombotic state identified by a significant increase in a polypeptide fragment and fibrinopeptide A was observed 3 hours after abruptly discontinuing heparin infusion. This observation may be clinically important in managing patients after coronary angioplasty. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. UNIV VERMONT,DEPT PATHOL,BURLINGTON,VT 05405. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 20 TC 25 Z9 25 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD MAR PY 1996 VL 131 IS 3 BP 434 EP 439 DI 10.1016/S0002-8703(96)90520-7 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA TZ295 UT WOS:A1996TZ29500002 PM 8604621 ER PT J AU Pratt, CM Ruberg, S Morganroth, J McNutt, B Woodward, J Harris, S Ruskin, J Moye, L AF Pratt, CM Ruberg, S Morganroth, J McNutt, B Woodward, J Harris, S Ruskin, J Moye, L TI Dose-response relation between terfenadine (Seldane) and the QTc interval on the scalar electrocardiogram: Distinguishing a drug effect from spontaneous variability SO AMERICAN HEART JOURNAL LA English DT Article ID TORSADES-DE-POINTES; KETOCONAZOLE; ASSOCIATION AB The primary goal of this investigation was to describe the effect of terfenadine on the QT interval corrected for heart rate (QTc) of the scalar electrocardiogram (EGG). The design was double-blind, four-period crossover, dose escalation, which involved 28 normal healthy volunteers and 28 patients with stable cardiovascular disease. At baseline, the normal subjects had a mean QTc interval of 407 msec, whereas the patients with cardiovascular disease had a mean QTc interval of 417 msec (p < 0.01). The largest increase in mean QTc on terfenadine was 24 msec in a normal subject and 28 msec in a patient with cardiovascular disease. The longest average QTc observed was 449 msec and 501 msec in any normal subject and patient with cardiovascular disease, respectively. Compared to baseline, terfenadine 60 mg twice daily is associated with a QTc increase of 6 msec in normal subjects and a 12 msec increase in patients with cardiovascular disease (p < 0.01 vs baseline; p > 0.05 when the two populations were compared). Although the QTc increases from baseline are statistically significant, the magnitude of the spontaneous variability in QTc in the same patients is much greater. Because 40 ECGs were obtained while taking placebo in each participant, the spontaneous variability in QTc interval with placebo was also described. Only one of the 28 normal subjects had a mean baseline QTc greater than or equal to 440 msec, yet 14 of the 28 normal subjects had at least one of the 40 placebo ECGs with a QTc greater than or equal to 440 msec. The 28 patients with cardiovascular disease had a mean QTc at baseline of 417 msec; yet 20 of 28 had at least one ECG on placebo with a QTc interval greater than or equal to 440 msec. On the average, the QTc fluctuated 56 msec in each patient during placebo administration. From the observed placebo variability, we calculated that an increase in QTc of greater than or equal to 35 msec while receiving drug therapy is likely to represent a drug effect at the 95% confidence interval. C1 PHILADELPHIA HEART INST,PHILADELPHIA,PA. UNIV PENN,PHILADELPHIA,PA 19104. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,HOUSTON,TX. RP Pratt, CM (reprint author), BAYLOR COLL MED,DEPT INTERNAL MED,CARDIOL SECT,6535 FANNIN MS F1001,HOUSTON,TX 77030, USA. NR 22 TC 101 Z9 104 U1 1 U2 4 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD MAR PY 1996 VL 131 IS 3 BP 472 EP 480 DI 10.1016/S0002-8703(96)90525-6 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA TZ295 UT WOS:A1996TZ29500007 PM 8604626 ER PT J AU Jiang, L Morrissey, R Handschumacher, MD dePrada, JAV Picard, MH Weyman, AE Levine, RA AF Jiang, L Morrissey, R Handschumacher, MD dePrada, JAV Picard, MH Weyman, AE Levine, RA TI Quantitative three-dimensional reconstruction of left ventricular volume with complete borders detected by acoustic quantification underestimates volume SO AMERICAN HEART JOURNAL LA English DT Article ID ULTRASONIC TISSUE CHARACTERIZATION; 3-DIMENSIONAL ECHOCARDIOGRAPHIC RECONSTRUCTION; AUTOMATIC BOUNDARY DETECTION; CANINE LEFT-VENTRICLE; INTEGRATED BACKSCATTER; GAIN COMPENSATION; ONLINE ASSESSMENT; STROKE VOLUME; MYOCARDIUM; VALIDATION AB Recently a new acoustic-quantification (AQ) technique has been developed to provide on-line automated border detection with an integrated backscatter analysis. Prior studies have largely correlated AQ areas with volumes without direct comparison of volumes for agreement. By using complete AQ-detected borders as the input to a validated method for three-dimensional echocardiographic (3DE) reconstruction, we can compare an entire cavity volume measured with the aid of AQ against a directly measured volume. This would also explore the possibility of applying AQ to 3DE reconstruction to reduce tracing time and enhance routine applicability. To compare reconstructed volumes with actual values in a stable standard allowing direct volume measurement, the left ventricles of 13 excised animal hearts were studied with a 3DE system that automatically combines two-dimensional (2D) images and their locations. Intersecting 2D views were obtained with conventional scanning and AQ imaging, with gains optimized to permit 3D reconstruction by detecting the most continuous AQ borders for each view, with maximal cavity size. Reconstruction was performed with manually traced central endocardial reflections and AQ-detected borders. 3DE reconstructions of both manually and AQ-detected borders visually reproduced the left ventricular shapes; the AQ reconstructions, however, were consistently smaller. The reconstructed left Ventricular (LV) volumes correlated well with actual values by both manual and AQ techniques (r = 0.93 and 0.88, with standard errors of 2.3 cc and 2.0 cc, p = not significant [NS]). Agreement with actual values was relatively close for the manually traced borders (y = 0.93x + 0.68, mean difference = -0.8 +/- 2.2 cc). AQ-derived reconstructions consistently underestimated LV volume by 39 +/- 10% (y = 0.62x - 0.09, mean difference = -7.8 +/- 3.0 cc, different from manually traced and actual volumes by analysis of variance [ANOVA], F = 69, p < 0.00001). The AQ-detected threshold signal was displaced into the cavity, and volume between walls and false tendons was excluded, leading to underestimation, which increased with increasing cavity volume (r = 0.76). The AQ technique can therefore be applied to 3DE reconstruction, providing volumes that correlate well with directly measured values in a stable in vitro standard, minimizing observer decisions regarding manual border placement after image acquisition. However, when the complete borders needed for 3D reconstruction are used, absolute volumes are underestimated with current algorithms that integrate backscatter and displace the detected threshold into the ventricular cavity. RP Jiang, L (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC ULTRASOUND LAB,VINCENT BURNHAM 5,FRUIT ST,BOSTON,MA 02114, USA. OI Picard, Michael/0000-0002-9264-3243 NR 66 TC 20 Z9 20 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD MAR PY 1996 VL 131 IS 3 BP 553 EP 559 DI 10.1016/S0002-8703(96)90536-0 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA TZ295 UT WOS:A1996TZ29500018 PM 8604637 ER PT J AU Erickson, LC Lopez, A Vlahakes, GJ King, ME Doody, DP Lang, P AF Erickson, LC Lopez, A Vlahakes, GJ King, ME Doody, DP Lang, P TI Massive intrahepatic shunting seen as severe cyanosis after the Fontan procedure in heterotaxy syndrome SO AMERICAN HEART JOURNAL LA English DT Article ID OPERATION C1 MASSACHUSETTS GEN HOSP,DIV CARDIOTHORAC SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT SURG,BOSTON,MA 02114. RP Erickson, LC (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT CARDIOL UNIT,VBK615 FRUIT ST,BOSTON,MA 02114, USA. NR 6 TC 6 Z9 6 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD MAR PY 1996 VL 131 IS 3 BP 608 EP 611 DI 10.1016/S0002-8703(96)90546-3 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA TZ295 UT WOS:A1996TZ29500028 PM 8604647 ER PT J AU Bliss, DZ Stein, TP Schleifer, CR Settle, RG AF Bliss, DZ Stein, TP Schleifer, CR Settle, RG TI Supplementation with gum arabic fiber increases fecal nitrogen excretion and lowers serum urea nitrogen concentration in chronic renal failure patients consuming a low-protein diet SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE gum arabic; fiber; chronic renal failure treatment; dietary therapy ID INTESTINAL BACTERIA; PROGRESSION; UREMIA; RESTRICTION; INSUFFICIENCY; METABOLISM; POPULATION; POTASSIUM; LACTULOSE; DIGESTION AB In chronic rend failure (CRF), plasma concentrations of the products of protein metabolism are increased. Current dietary management is to prescribe a decrease in protein intake. The use of dietary fiber to increase feed excretion of retained metabolites in CRF may be a beneficial adjunct to a low-protein diet (LPD). Colonic bacteria ferment dietary fiber, providing them with energy for growth and nitrogen incorporation, in turn, increasing nitrogen excretion in feces. Sixteen CRF patients consuming an LPD were randomly assigned to receive a supplement of a highly fermentable fiber, gum arabic (50 g/d), or a placebo (1 g pectin/d) in a prospective, single-blind, crossover design. Fecal bacterial mass and fecal nitrogen content were significantly increased during supplementation with gum arabic compared with the baseline LPD or supplementation with pectin. Serum urea nitrogen was significantly decreased during supplementation with gum arabic compared with the baseline LPD or supplementation with pectin. Nitrogen balance did not change significantly. C1 UNIV PENN,SCH NURSING,PHILADELPHIA,PA 19104. UNIV PENN,DEPT OTORHINOLARYNGOL,PHILADELPHIA,PA 19104. UNIV MED & DENT NEW JERSEY,STRATFORD,NJ. LANKENAU HOSP,DEPT NEPHROL,WYNNEWOOD,OK. PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP Bliss, DZ (reprint author), UNIV MINNESOTA,SCH NURSING,6-101 HS UNIT F,308 HARVARD ST SE,MINNEAPOLIS,MN 55455, USA. NR 61 TC 68 Z9 70 U1 1 U2 2 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD MAR PY 1996 VL 63 IS 3 BP 392 EP 398 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA TY524 UT WOS:A1996TY52400018 PM 8602598 ER PT J AU Remsen, LG McCormick, CI RomanGoldstein, S Nilaver, G Weissleder, R Bogdanov, A Hellstrom, KE Hellstrom, I Kroll, RA Neuwelt, EA AF Remsen, LG McCormick, CI RomanGoldstein, S Nilaver, G Weissleder, R Bogdanov, A Hellstrom, KE Hellstrom, I Kroll, RA Neuwelt, EA TI MR of carcinoma-specific monoclonal antibody conjugated to monocrystalline iron oxide nanoparticles: The potential for noninvasive diagnosis SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE antigens and antibodies; brain neoplasms; magnetic resonance; carcinoma; animal studies ID METASTASES; BRAIN; SURGERY; TRIAL AB PURPOSE: To determine if tumor-specific monoclonal antibodies conjugated to superparamagnetic monocrystalline iron oxide nanoparticles can be used to yield specific diagnoses with the use of MR imaging. METHODS: Monoclonal antibodies conjugated to monocrystalline iron oxide nanoparticles were given to nude rats with intracranial tumors either by intravenous injection, intraarterial injection with osmotic blood-brain barrier disruption, or direct intratumoral inoculation. Either L6, a tumor-specific antibody, or P-1.17, a control isotype-matched antibody, was used. Coronal T1-weighted, T2-weighted, and spoiled gradient-recalled acquisition in the steady state images were obtained before, 30 minutes after, 6 hours after, and 24 hours after injection. RESULTS: Intravenous injection of greater than 2 mg of the tumor-specific antibody showed a specific pattern of enhancement of the tumors with the largest concentration of antibody in the area with the greatest density of tumor cells. The control antibody showed nonspecific changes. After intraarterial injection with barrier disruption to increase delivery globally or direct inoculation to increase delivery focally, no specific enhancement pattern was seen. CONCLUSION: Monoclonal antibodies conjugated with monocrystalline iron oxide particles may provide a method to obtain specific diagnoses with the use of MR imaging. C1 OREGON HLTH SCI UNIV,DEPT NEUROL L603,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT BIOCHEM & MOLEC BIOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT RADIOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT CELL BIOL & ANAT,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT OPHTHALMOL,PORTLAND,OR 97201. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,SEATTLE,WA. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,NMR CTR,DEPT RADIOL,BOSTON,MA. VET ADM MED CTR,PORTLAND,OR. FU NCI NIH HHS [CA59649, CA59649-01]; NINDS NIH HHS [NS27757] NR 24 TC 94 Z9 100 U1 0 U2 2 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD MAR PY 1996 VL 17 IS 3 BP 411 EP 418 PG 8 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA UB139 UT WOS:A1996UB13900005 PM 8881233 ER PT J AU GeifmanHoltzman, O Bernstein, IM Berry, SM Holtzman, EJ Vadnais, TJ DeMaria, MA Bianchi, DW AF GeifmanHoltzman, O Bernstein, IM Berry, SM Holtzman, EJ Vadnais, TJ DeMaria, MA Bianchi, DW TI Fetal RhD genotyping in fetal cells flow sorted from maternal blood SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY LA English DT Article DE fetal cells in maternal blood; polymerase chain reaction; RhD blood type; fluorescence-activated cell sorting ID PRENATAL DETERMINATION; DNA AB OBJECTIVE: The aim of this study was to determine the accuracy of noninvasive fetal RhD genotyping by fetal cell isolation from maternal blood. STUDY DESIGN: Candidate fetal cells from 18 pregnant women (one twin gestation) were flow-sorted. Polymerase chain reaction amplification of a 261 bp fragment of the RhD gene was performed on sorted fetal cells. The presence of amplified product was considered predictive of the RhD-positive genotype in the fetus. RESULTS: Sixteen of the 19 fetal RhD genotypes were correctly predicted in fetal cells isolated from maternal blood (10 were Rh positive, 6 were Rh negative). In 3 cases no amplification products were detected in RhD-positive fetuses. The association between presence of the fragment and RhD-positive genotype was significant (p = 0.003, Fisher's exact test). CONCLUSIONS: Noninvasive prenatal diagnosis of the fetal RhD genotype is feasible. Absence of amplification products in the reaction requires confirmation that fetal material is present. Improvements in fetal cell purity and yield should increase diagnostic accuracy, although the current protocol has a positive predictive value of 100% and a negative predictive value of 67%. C1 TUFTS UNIV,NEW ENGLAND MED CTR,DEPT PEDIAT,BOSTON,MA 02111. TUFTS UNIV,NEW ENGLAND MED CTR,DEPT OBSTET & GYNECOL,BOSTON,MA 02111. MED CTR HOSP VERMONT,DIV MATERNAL FETAL MED,BURLINGTON,VT. HUTZEL HOSP,DIV MATERNAL FETAL MED,DETROIT,MI 48201. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 17 TC 49 Z9 51 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-9378 J9 AM J OBSTET GYNECOL JI Am. J. Obstet. Gynecol. PD MAR PY 1996 VL 174 IS 3 BP 818 EP 822 DI 10.1016/S0002-9378(96)70306-X PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA UC866 UT WOS:A1996UC86600004 PM 8633649 ER PT J AU Nageris, B Adams, JC Merchant, SN AF Nageris, B Adams, JC Merchant, SN TI A human temporal bone study of changes in the basilar membrane of the apical turn in endolymphatic hydrops SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article; Proceedings Paper CT 128th Annual Meeting of the American-Otological-Society CY APR 29-30, 1995 CL PALM DESERT, CA SP Amer Otol Soc DE temporal bone; basilar membrane; apical turn; hydrops, endolymphatic; sensorineural hearing loss AB We observed that some temporal bones with endolymphatic hydrops (EH) showed varying degrees of basalward displacement (towards the scala tympani) of the basilar membrane (BM) in the apical turn of the cochlea. In some, the BM was adherent to the bony wall of the scala tympani (i.e., the interscalar septum). Such mechanical distortion of the BM could conceivably alter cochlear mechanics and lead to sensorineural hearing loss. The results of a systematic evaluation of 234 temporal bones to characterize, quantify and determine the functional significance of this observation are presented. Four groups of bones were evaluated: normal (N = 78), presbycusis (N = 96), Meniere's disease (N = 23), and EH secondary to labyrinthitis (N = 37). The incidence of extreme displacement of the BM in the apical turn such that it adhered to the interscalar septum was 52% in Meniere's disease, 57% in EH secondary to labyrinthitis, 10% in presbycusis, and 1% in normals. These differences were significant and could not be explained on the basis of age, sex, post-mortem time, or artifact of technique or processing. Displacement of the BM was not observed in other turns of the cochlea. Its pathogenesis is not known, but may be related to atrophy of the spiral ligament. It is likely that such BM displacement results in sensorineural hearing loss. However, our data and theoretical analyses both indicate that such a loss will be restricted to frequencies below 100 Hz and that this pathologic change alone is not likely to cause appreciable hearing loss at clinically tested frequencies of 250 Hz and higher. Hence, even though this pathologic finding is common in endolymphatic hydrops, it cannot explain the low-frequency hearing loss observed in Meniere's disease. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. FU NIDCD NIH HHS [R01 DC00079] NR 5 TC 8 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD MAR PY 1996 VL 17 IS 2 BP 245 EP 252 PG 8 WC Otorhinolaryngology SC Otorhinolaryngology GA UJ075 UT WOS:A1996UJ07500016 PM 8723956 ER PT J AU McKenna, MJ Nadol, JB Ojemann, RG Halpin, C AF McKenna, MJ Nadol, JB Ojemann, RG Halpin, C TI Vestibular neurectomy: Retrosigmoid-intracanalicular versus retrolabyrinthine approach SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article DE vestibular neurectomy; retrolabyrinthine; retrosigmoid; internal auditory canal ID NERVE-SECTION AB Selective vestibular neurectomy is an effective treatment for intractable vertigo of peripheral vestibular origin when preservation of hearing is a goal. The retrolabyrinthine and retrosigmoid-intracanalicular approaches have been used predominantly at our institutions over the last 10 years. The results and complications of these two techniques were compared. No significant differences were found between hearing results in these two patient groups. The retrosigmoid-internal auditory canal approach yielded better control of recurrent episodic vertigo, as well as superior ablation of postoperative ice-water caloric responses (p < 0.05). Surgical complications, including the incidence of cerebrospinal fluid leakage (greater in retrolabyrinthine approach) and postoperative headache (more prevalent in retrosigmoid approach), were also analyzed. To further evaluate the results of this study, data were reanalyzed and compared with previously published reports of selective vestibular nerve section. C1 HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. RP McKenna, MJ (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOL & LARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 22 TC 19 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD MAR PY 1996 VL 17 IS 2 BP 253 EP 258 PG 6 WC Otorhinolaryngology SC Otorhinolaryngology GA UJ075 UT WOS:A1996UJ07500017 PM 8723957 ER PT J AU Saim, L Nadol, JB AF Saim, L Nadol, JB TI Vestibular symptoms in otosclerosis - Correlation of otosclerotic involvement of vestibular apparatus and Scarpa's ganglion cell count SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article DE Scarpa's ganglion; vestibule; otosclerosis AB Although several histopathologic studies have shown otosclerotic involvement of the vestibular apparatus in patients with otosclerosis, the pathogenesis of vestibular symptoms in otosclerosis remains unknown. A quantitative study of Scarpa's ganglion was performed in 217 temporal bones from 118 subjects with otosclerosis. Review of clinical records revealed an incidence of vestibular symptoms in 11.9% of these subjects. Scarpa's ganglion cell counts in temporal bones of subjects with otosclerosis and vestibular symptoms were lower than counts in temporal bones of subjects with otosclerosis but without vestibular symptoms and those of normal subjects. This difference in Scarpa's ganglion cell counts, adjusted for age, between the group with otosclerosis and vestibular symptoms and a group of normal subjects was highly significant (p = 0.0015), whereas the difference in Scarpa's ganglion cell count between a group with otosclerosis but without vestibular symptoms and a group of normal subjects was not significant (p = 0.53). There was also a significant correlation between elevation of the average bone-conduction threshold and the presence of vestibular symptoms in these subjects (p = 0.041). The endosteum of the perilymphatic space of the vestibule and the endosteum of the canal for the superior vestibular nerve or its cribrose area were the two most common sites of involvement by otosclerosis. However, there was no significant correlation between the presence of vestibular symptoms and otosclerotic involvement of any single site or the number of involved sites. Histologic examination of the vestibular nerve fibers and end organs subjacent to otosclerotic foci demonstrated no obvious degenerative changes. Thus our findings appear to suggest that the vestibular symptoms present in patients with otosclerosis are more common in patients with elevated bone conduction thresholds and are correlated with degeneration of the vestibular nerve, which appears to be independent of the severity of otosclerotic involvement of the vestibular end organs. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. FU NIDCD NIH HHS [5 RO1 DC 00079] NR 24 TC 8 Z9 9 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD MAR PY 1996 VL 17 IS 2 BP 263 EP 270 PG 8 WC Otorhinolaryngology SC Otorhinolaryngology GA UJ075 UT WOS:A1996UJ07500019 PM 8723959 ER PT J AU Nadol, JB Diamond, PF Thornton, AR AF Nadol, JB Diamond, PF Thornton, AR TI Correlation of hearing loss and radiologic dimensions of vestibular schwannomas (acoustic neuromas) SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article DE acoustic neuroma; sensorineural hearing loss; tumor size ID PRESERVATION; DIAGNOSIS; SURGERY AB A retrospective analysis was performed of pure-tone audiograms, speech-discrimination scores, and gadolinium-enhanced magnetic resonance imaging scans of 75 patients with vestibular schwannomas (acoustic neuroma). Sensorineural hearing loss was analyzed for low frequencies (250-500 Hz), midfrequencies (1,000-2,000 Hz), and high frequencies (4,000-8,000 Hz). The largest tumor diameter in the cerebellopontine angle and the lateral extent of invasion by tumor into the internal auditory canal were calculated from magnetic resonance images. There were statistically significant correlations between the largest tumor diameter and the severity of low-frequency sensorineural heaing loss (p = 0.001). However, no significant correlations were found between the following: largest tumor diameter and the severity of mid-frequency or high-frequency sensorineural hearing loss or speech-discrimination scores and lateral extent of invasion of the internal auditory canal and sensorineural hearing loss at all frequencies or speech-discrimination scores (p greater than or equal to 0.05). The findings suggest that nerve compression is not the only cause of hearing loss in vestibular schwannoma. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. RP Nadol, JB (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 30 TC 32 Z9 32 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD MAR PY 1996 VL 17 IS 2 BP 312 EP 316 PG 5 WC Otorhinolaryngology SC Otorhinolaryngology GA UJ075 UT WOS:A1996UJ07500028 PM 8723968 ER PT J AU Saim, L McKenna, HJ Nadol, JB AF Saim, L McKenna, HJ Nadol, JB TI Tubal and tympanic openings of the peritubal cells: Implications for cerebrospinal fluid otorhinorrhea SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article DE mastoid air cells; cerebrospinal fluid leak; rhinorrhea; cerebellopontine angle surgery ID ACOUSTIC NEUROMA SURGERY; CEREBELLOPONTINE ANGLE; TUMOR SURGERY; MENINGITIS; LEAKS; COMPLICATIONS; MANAGEMENT; REPAIR AB Cerebrospinal fluid otorhinorrhea after surgery for cerebellopontine angle tumors may persist despite obliteration of the mastoid, middle ear, and tympanic orifice of the eustachian tube. In this study, histologic sections of 120 adult temporal bones were examined by light microscopy to determine the incidence of peritubal pneumatization and to demonstrate the frequency of tubal and tympanic openings of the peritubal cells. The results of this study suggest that the pathway for these persistent cerebrospinal fluid leaks may be via the peritubal cells that open directly into the eustachian tube anterior to its tympanic orifice. Peritubal pneumatization was present in 78 (65%) of the temporal bones. Of the 57 specimens in which the openings of the peritubal cells could be identified, in 52 (91%), the cells opened into the eustachian tube anterior to its tympanic orifice, and in only five (9%), they opened into the middle ear. The overall incidence of tubal openings in this study was 59%. In 13 temporal bones (21%), the tubal openings were at a distance of >5 mm anterior to the tympanic orifice of the eustachian tube. Therefore, cerebrospinal leak may persist through these tubal, openings despite obliteration of the mastoid, middle ear, and tympanic orifice of the eustachian tube. A case of persistent cerebrospinal fluid leak in which extensive peritubal pneumatization was demonstrated by computed tomography scan is presented. Successful control of the leak was obtained only after the tubal openings of these cells several millimeters anterior to the tympanic orifice were obliterated. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. FU NIDCD NIH HHS [5 RO1 DC 00079] NR 24 TC 14 Z9 14 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD MAR PY 1996 VL 17 IS 2 BP 335 EP 339 PG 5 WC Otorhinolaryngology SC Otorhinolaryngology GA UJ075 UT WOS:A1996UJ07500032 PM 8723972 ER PT J AU Nguyen, PL Harris, NL Ritz, J Robertson, MJ AF Nguyen, PL Harris, NL Ritz, J Robertson, MJ TI Expression of CD95 antigen and Bcl-2 protein in non-Hodgkin's lymphomas and Hodgkin's disease SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID TUMOR-NECROSIS-FACTOR; GROWTH-FACTOR RECEPTOR; CELL-SURFACE ANTIGEN; MOLECULAR-CLONING; FAS ANTIGEN; MONOCLONAL-ANTIBODY; MEDIATED APOPTOSIS; APO-1 ANTIGEN; MEMBER; FAMILY AB CD95 (APO-1/Fas) is a member of the superfamily that includes the nerve growth factor and tumor necrosis factor receptors, OX40, CD27, CD30, and CD40. Present on a minority of resting blood lymphocytes, CD95 expression is upregulated on activated T and B lymphocytes and natural killer cells, where binding of the antigen by anti-Pas and anti-APO-1 antibodies has been shown to induce apoptosis. This CD95-mediated apoptosis is at least partially inhibited by expression of the Bcl-2 protooncogene. To evaluate possible roles of CD95 and Bcl-2 in growth regulation of lymphoid neoplasms, we studied by immunohistochemistry the expression of CD95 and Bcl-2 in 67 B- and 5 T-cell lymphomas, and 10 cases of Hodgkin's disease In all, 29 B and 2 T cell lymphomas, and 9 cases of Hodgkin's disease expressed CD95. Compared with diffuse large B-cen and Burkitt-like Lymphomas, low-grade B-cell lymphomas more frequently expressed CD95 (52% versus 26%; P < .005). None of the B-cell small lymphocytic lymphomas or mantle cell lymphomas expressed CD95, whereas the majority of follicle center lymphomas, extranodal marginal zone B-cea lymphomas, and immunocytomas were CD95(+). Of the 29 CD95(+) B-cell lymphomas, only 33% of the high-grade group coexpressed Bcl-2, compared with 87% of the low-grade group CP < .04). Two of three peripheral T-cell lymphomas-including one anaplastic large cell lymphoma-expressed CD95. Staining for CD95 was seen in 9 of 10 cases of Hodgkin's disease The infrequent expression of CD95 in high-grade B-cell lymphomas suggests an association between loss of CD95 expression/function and a more aggressive tumor grade. Whereas frequent coexpression of Bcl-2 with CD95 may protect low-grade B-cell lymphomas against CD95-mediated apoptosis, in the high-grade group such coexpression is infrequent, and other regulators besides Bcl-2 may be involved in modulating the apoptosis signal delivered by CD95. C1 HARVARD UNIV,SCH MED,DIV HEMATOL MALIGNANCIES,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP Nguyen, PL (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,WARREN 2,32 FRUIT ST,BOSTON,MA 02114, USA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 NR 34 TC 62 Z9 63 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD MAR PY 1996 VL 148 IS 3 BP 847 EP 853 PG 7 WC Pathology SC Pathology GA TY074 UT WOS:A1996TY07400018 PM 8774139 ER PT J AU Spielman, AI Nagai, H Sunavala, G Dasso, M Breer, H Boekhoff, I Huque, T Whitney, G Brand, JG AF Spielman, AI Nagai, H Sunavala, G Dasso, M Breer, H Boekhoff, I Huque, T Whitney, G Brand, JG TI Rapid kinetics of second messenger production in bitter taste SO AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY LA English DT Article DE gustatory; quench flow; G proteins ID ADENYLATE-CYCLASE; SUCROSE STIMULATION; TRANSDUCTION; AMILORIDE; CELLS; RESPONSES; MEMBRANES; CALCIUM; LOCALIZATION; CHANNELS AB The tasting of bitter compounds may have evolved as a protective mechanism against ingestion of potentially harmful substances. We have identified second messengers involved in bitter taste and show here for the first time that they are rapid and transient. Using a quench-flow system, we have studied bitter taste signal transduction in a pair of mouse strains that differ in their ability to taste the bitter stimulus sucrose octaacetate (SOA); however, both strains taste the bitter agent denatonium. In both strains of mice, denatonium (10 mM) induced a transient and rapid increase in levels of the second messenger inositol 1,4,5-trisphosphate (IP3) with a maximal production near 75-100 ms after stimulation. In contrast, SOA (100 mu M) brought about a similar increase in IP3 only in SOA-taster mice. The response to SOA was potentiated in the presence of GTP (1 mu M) The GTP-enhanced SOA-response supports a G protein-mediated response for this bitter compound. The rapid kinetics, transient nature, and specificity of the bitter taste stimulus-induced IP3 formation are consistent with the role of IP3 as a second messenger in the chemoelectrical transduction of bitter taste. C1 UNIV PENN, SCH DENT MED, DEPT BIOCHEM, PHILADELPHIA, PA 19104 USA. UNIV PENN, MONELL CHEM SENSES CTR, PHILADELPHIA, PA 19104 USA. VET AFFAIRS MED CTR, PHILADELPHIA, PA 19104 USA. FLORIDA STATE UNIV, DEPT PSYCHOL, TALLAHASSEE, FL 32306 USA. SUNTORY LTD, INST FUNDAMENTAL RES, OSAKA 618, JAPAN. UNIV STUTTGART HOHENHEIM, DEPT ZOOPHYSIOL, W-7000 STUTTGART 70, GERMANY. RP Spielman, AI (reprint author), NYU, COLL DENT, DIV BASIC SCI, NEW YORK, NY 10010 USA. NR 33 TC 56 Z9 56 U1 1 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6143 J9 AM J PHYSIOL-CELL PH JI Am. J. Physiol.-Cell Physiol. PD MAR PY 1996 VL 270 IS 3 BP C926 EP C931 PG 6 WC Cell Biology; Physiology SC Cell Biology; Physiology GA UA603 UT WOS:A1996UA60300027 PM 8638676 ER PT J AU Saydoff, JA Rittenhouse, PA Carnes, M Armstrong, J vandeKar, LD Brownfield, MS AF Saydoff, JA Rittenhouse, PA Carnes, M Armstrong, J vandeKar, LD Brownfield, MS TI Neuroendocrine and cardiovascular effects of serotonin: Selective role of brain angiotensin on vasopressin SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM LA English DT Article DE 5-hydroxytryptamine; d-fenfluramine; enalapril; losartan; intracerebroventricular; rat ID CONVERTING ENZYME; CONSCIOUS RATS; RAPHE SYSTEM; SECRETION; RELEASE; OXYTOCIN; PRESSOR; AT1-RECEPTOR; AT2-RECEPTOR; TRANSMISSION AB Central serotonin (5-HT) and angiotensin (ANG II) stimulate arginine vasopressin (AVP), oxytocin (OT), and adrenocorticotropin (ACTH) secretion and increase blood pressure. Studies were conducted in conscious rats to determine whether neuroendocrine activation by 5-HT requires a brain angiotensinergic intermediate pathway. In the first study, ANG LI formation was inhibited by the angiotensin-converting enzyme inhibitor enalapril before injection of the 5-HT releaser/uptake inhibitor d-fenfluramine. Fenfluramine (2 mg/kg ip) stimulated AVP, OT, corticosterone, and prolactin (PRL) secretion (P < 0.01). Enalapril (60 mg/l in drinking water for 4 days and 10 mg/kg ip 2 h before rats were killed) inhibited only the AVP response (P < 0.01) to d-fenfluramine. In the second study, the effect of intracerebroventricular injection of the 5-HT2A/2C antagonist LY-53857 (10 mu g), or the ANG II AT(1) antagonist DuP-753 (10 mu g), on intracerebroventricular 5-HT (10 mu g)stimulated AVP, OT, ACTH, PRL, renin secretion, mean arterial pressure (MAP) and heart rate (HR) was tested. LY-53857 inhibited the AVP, OT, and ACTH responses to 5-HT (P < 0.01), whereas DuP-753 inhibited only the AVP response (P < 0.01). Intraventricular injection of 5-HT increased MAP and decreased HR. The MAP response was not affected by LY-53857 or DuP-753, and at no time did MAP decline below starting levels. The decreased HR was inhibited by LY-53857 but not by DuP-753. These results demonstrate that 5-HT-induced AVP secretion is mediated selectively via brain angiotensinergic mechanisms by way of the AT(1) receptor. C1 UNIV WISCONSIN, DEPT COMPARAT BIOSCI, RADIOIMMUNOASSAY & RADIONUCLIDE LAB, MADISON, WI 53706 USA. UNIV WISCONSIN, SCH VET MED, DEPT MED, MADISON, WI 53706 USA. UNIV WISCONSIN, SCH MED, MADISON, WI 53706 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, CTR GERIATR RES EDUC & CLIN, MADISON, WI 53706 USA. LOYOLA UNIV, STRITCH SCH MED, DEPT PHARMACOL & EXPTL THERAPEUT, MAYWOOD, IL 60153 USA. FU NIDDK NIH HHS [R29-DK-40759]; NIMH NIH HHS [MH-45812] NR 33 TC 34 Z9 36 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1849 J9 AM J PHYSIOL-ENDOC M JI Am. J. Physiol.-Endocrinol. Metab. PD MAR PY 1996 VL 270 IS 3 BP E513 EP E521 PG 9 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA UA593 UT WOS:A1996UA59300020 PM 8638700 ER PT J AU Ma, JY Ayata, C Huang, PL Fishman, MC Moskowitz, MA AF Ma, JY Ayata, C Huang, PL Fishman, MC Moskowitz, MA TI Regional cerebral blood flow response to vibrissal stimulation in mice lacking type I NOS gene expression SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE nitric oxide; type I nitric oxide synthase; transgenic mice; whisker stimulation; N omega-nitro-L-arginine ID NITRIC-OXIDE; NERVE STIMULATION; L-ARGININE; RAT; INHIBITION; MICROCIRCULATION; ORGANIZATION; VASOMOTION; INDUCTION; BRAIN AB The role of nitric oxide (NO) in cerebral blood flow-metabolism coupling was assessed in SV-129 wild-type (WT) and neuronal (type I) NO synthase (NOS) knockout mice (Kn). Regional cerebral blood flow (rCBF; laser-Doppler flowmetry) was measured over the contralateral cortical barrel field during unilateral mechanical vibrissal deflection (2-3 Hz, 60 s) under urethan anesthesia. The rCBF response was similar in WT and Kn and did not differ when recorded over the intact skull or closed cranial window preparations. Whisker stimulation increased rCBF by 41 +/- 8% (maximum) and 27 +/- 6% (mean) in WT (n = 6) and 41 +/- 7% (maximum) and 26 +/- 6% (mean) in Kn (n = 6) when recorded through a closed cranial window. After superfusion with topical N-omega-nitro-L-arginine (L-NNA; 1 mM), the rCBF response was inhibited by similar to 45% in WT mice (P < 0.05), whereas there was no inhibition in Kn. Endothelium-dependent relaxation, assessed by pial vessel dilation in response to topical acetylcholine (100 mu M) and inhibition by L-NNA (1 mM), was the same in both groups. Our results suggest that 1) endothelial NO production does not mediate the rCBF coupling to neuronal activity in Kn, 2) the inhibitory effect of L-NNA on the rCBF response to whisker stimulation in WT is a consequence of type I (neuronal) NOS inhibition, and 3) NO-independent mechanisms couple rCBF and metabolism during whisker stimulation in mice lacking expression of neuronal NOS. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV, STROKE & NEUROVASC REGULAT LAB, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG, NEUROL DEPT, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,MED SERV, CARDIOVASC RES CTR, BOSTON, MA 02114 USA. RI Moskowitz, Michael/D-9916-2011 NR 33 TC 99 Z9 99 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD MAR PY 1996 VL 270 IS 3 BP H1085 EP H1090 PG 6 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA UA049 UT WOS:A1996UA04900035 ER PT J AU Katsura, T Ausiello, DA Brown, D AF Katsura, T Ausiello, DA Brown, D TI Direct demonstration of aquaporin-2 water channel recycling in stably transfected LLC-PK1 epithelial cells SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article DE vasopressin; forskolin; endocytosis; exocytosis; vesicle trafficking ID DUCT PRINCIPAL CELLS; ANTIDIURETIC-HORMONE; COLLECTING DUCT; RAT-KIDNEY; COATED PITS; ENDOCYTOSIS; TRANSPORT; TUBULE AB Vasopressin-dependent membrane insertion of aquaporin-2 (AQP-2) in collecting duct principal cells has been demonstrated in vivo and in vitro. However, the hypothesis that the AQP-2 molecule recycles between intracellular vesicles and the plasma membrane in response to hormonal stimulation and withdrawal remains to he demonstrated directly. In the present study, we examined AQP-2 recycling between intracellular vesicles and the plasma membrane in the absence of de novo protein synthesis using LLC-PK1 cells transfected with an AQP-2-c-myc construct. Cells were treated with cycloheximide for 30 min prior to vasopressin stimulation, and all subsequent treatments were performed in the continued presence of cycloheximide. Complete inhibition of AQP-2 biosynthesis by cycloheximide was verified by immunoprecipitation. Immunofluorescence revealed that AQP-2 was located on intracellular vesicles in stimulated cells but was relocated to the plasma membrane after vasopressin treatment, even in the presence of cycloheximide. After vasopressin washout, AQP-2 was retrieved to intracellular vesicles and was relocated to;the plasma membrane after restimulation with forskolin. Subsequent forskolin washout resulted in AQP-2 endocytosis, and a second stimulation with forskolin resulted in relocation to the plasma membrane. These data, obtained in the absence of de novo protein synthesis, clearly indicate that AQP-2 can be recycled multiple times between intracellular vesicles and the plasma membrane. C1 MASSACHUSETTS GEN HOSP, RENAL UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [DK-38452] NR 31 TC 71 Z9 73 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrolyte Physiol. PD MAR PY 1996 VL 270 IS 3 BP F548 EP F553 PG 6 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA UA048 UT WOS:A1996UA04800022 PM 8780259 ER PT J AU Pollack, MH Otto, MW Sabatino, S Majcher, D Worthington, JJ McArdle, ET Rosenbaum, JF AF Pollack, MH Otto, MW Sabatino, S Majcher, D Worthington, JJ McArdle, ET Rosenbaum, JF TI Relationship of childhood anxiety to adult panic disorder: Correlates and influence on course SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID BEHAVIORAL-INHIBITION; SEPARATION ANXIETY; LONGITUDINAL COURSE; YOUNG-CHILDREN; SCHOOL PHOBIA; AGORAPHOBIA; FAMILY; PARENTS; RISK; COMORBIDITY AB Objective: This study investigated the correlates of a childhood history of anxiety disorders in adult patients participating in a longitudinal study of panic disorder. The authors hypothesized that a history of anxiety during childhood would be associated with higher rates of comorbid anxiety and depressive disorders, greater likelihood of anxiety disorders in family members, and greater chronicity, as reflected by decreased time spent in remission. Method: The presence of a childhood history of anxiety disorders was assessed by structured interview, and its association with comorbid anxiety and depressive disorders, family history, and select anxiety severity, variables was examined in a replication sample of 94 patients. The influence of childhood anxiety on the prospectively ascertained course of disorder was assessed in a full group of 194 patients. Results: Over half (54%) of the patients experienced anxiety disorders during childhood. These patients experienced higher rates of comorbid anxiety and depression, family history of anxiety, and increased levels of agoraphobia, panic frequency, and global severity of illness at baseline evaluation. Childhood anxiety disorders were not independently associated with the number of months in remission or the severity of illness over time, although a modest effect for this variable was evident when degree of avoidance and anxiety sensitivity at baseline were statistically controlled. Conclusions: Adult panic patients with a history of anxiety disorders in childhood have elevated rates of comorbid anxiety and depressive disorders and a tendency toward increased avoidance, but there was not strong evidence that these patients respond differently to treatment over time. RP Pollack, MH (reprint author), MASSACHUSETTS GEN HOSP,ANXIETY DISORDERS PROGRAM,ACC-815,15 PARKMAN ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH-196000] NR 35 TC 75 Z9 81 U1 1 U2 4 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAR PY 1996 VL 153 IS 3 BP 376 EP 381 PG 6 WC Psychiatry SC Psychiatry GA TY356 UT WOS:A1996TY35600011 PM 8610825 ER PT J AU Imanaka, H Kacmarek, RM Ritz, R Hess, D AF Imanaka, H Kacmarek, RM Ritz, R Hess, D TI Tracheal gas insufflation pressure control versus volume control ventilation - A lung model study SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID CONSTANT-FLOW VENTILATION; DOGS; CATHETER; EXCHANGE AB Tracheal gas insufflation (TCI) has been recommended as an adjunct to mechanical ventilation in the presence of elevated Pa-CO2. Based on our initial clinical experience with continuous flow TGI and pressure control ventilation (PCV), we were concerned about elevation in peak airway pressure as TCI was applied. In a lung model, we evaluated the effects of continuous flow TCI during both PCV and volume control ventilation (VCV). A single compartment lung model was configured with an artificial trachea into which an 8-mm endotracheal tube was positioned. TCI was established with a 16-G catheter positioned 2 cm beyond the tip of the endotracheal tube. Ventilation was provided by a Puritan-Bennett 7200ae ventilator with PCV 20 cm H2O or VCV with a tidal volume (VT) similar to that with PCV. A rate of 15 breaths/min and PEEP of 10 cm H2O were used throughout. Inspiratory times (TI) of 1.0, 1.5, 2.0, and 2.5 s were used with TCI of 0, 4, 8, and 12 L/min. Lung model compliance (ml/cm H2O) and resistance (cm H(2)0/L/s) combinations of 20/20, 20/5, and 50/20 were used. Auto-PEEP, VT, and peak alveolar and airway opening pressures increased as TCI and TI increased, regardless of lung mechanics settings (p < 0.01). All increases were greater with VCV than PCV (p < 0.05). Continuous flow TCI with both PCV and VT-uncorrected VCV may result in marked increases in VT and system pressures, especially at long TI. C1 MASSACHUSETTS GEN HOSP,RESP CARE DEPT LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 19 TC 21 Z9 22 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD MAR PY 1996 VL 153 IS 3 BP 1019 EP 1024 PG 6 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA TY527 UT WOS:A1996TY52700022 PM 8630540 ER PT J AU Bozic, CR Gerard, NP Gerard, C AF Bozic, CR Gerard, NP Gerard, C TI Receptor binding specificity and pulmonary gene expression of the neutrophil-activating peptide ENA-78 SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID RESPIRATORY-DISTRESS-SYNDROME; HUMAN INTERLEUKIN-8 RECEPTOR; GROWTH-STIMULATORY ACTIVITY; CYSTIC-FIBROSIS; INFLAMMATORY CYTOKINES; FAMILY; DISEASES; BIOLOGY; SPUTUM AB Neutrophil-activating peptide ENA-78 is a novel chemotactic cytokine isolated from a human type II pulmonary epithelial cell line. It is a member of the chemokine family of proinflammatory polypeptides and exhibits structural homology to interleukin-8 (IL-8) and GRO alpha. The immunohistochemical identification of ENA-78 in pulmonary alveolar leukocytes of bovine pneumonic lungs supports a role for ENA-78 in the pathogenesis of pulmonary inflammation. Although ENA-78 is able to stimulate polymorphonuclear neutrophils (PMN), neither its binding specificities nor its expression in human pulmonary disease states have been determined. I-125-labeled ENA-78 binds with high affinity to human PMN. Its actions on PMN appear to be mediated by the IL-8 type B receptor, to which it binds with a K-d of 2.2 nM. Human IL-8, GRO alpha, and murine KC compete with high affinity for I-125-ENA-78 binding to the human IL-8 type B receptor. In contrast, I-125-ENA-78 does not bind to the IL-8 type A receptor nor does it compete significantly for I-125-IL-8 binding to this same receptor. ENA-78 is a potent upregulator of Mac-1 cell surface expression. In addition, ENA-78 mRNA is detected in cystic fibrosis lung but is not detected in normal donor lung. Thus, ENA-78 mRNA levels appear to be increased in human pulmonary inflammation and its stimulatory activities on PMN appear to be a function mediated primarily by the IL-8 type B receptor. C1 CHILDRENS HOSP, DEPT PEDIAT, INA SUE PERLMUTTER LAB, BOSTON, MA USA. BETH ISRAEL HOSP, DEPT MED, BOSTON, MA 02215 USA. BRIGHAM & WOMENS HOSP, DEPT MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, CTR BLOOD RES, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, THORNDIKE LAB, BOSTON, MA 02115 USA. FU NHLBI NIH HHS [HL-71910, HL-36162] NR 41 TC 26 Z9 26 U1 0 U2 2 PU AMER THORACIC SOC PI NEW YORK PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD MAR PY 1996 VL 14 IS 3 BP 302 EP 308 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA TY727 UT WOS:A1996TY72700013 PM 8845182 ER PT J AU Boland, GW Mueller, PR Lee, MJ AF Boland, GW Mueller, PR Lee, MJ TI Laparoscopic cholecystectomy with bile duct injury: Percutaneous management of biliary stricture and associated complications SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Discussion ID DILATATION C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. NR 10 TC 4 Z9 4 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAR PY 1996 VL 166 IS 3 BP 603 EP 607 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TW774 UT WOS:A1996TW77400021 PM 8623635 ER PT J AU Spillane, RM Whitman, GJ Chew, FS AF Spillane, RM Whitman, GJ Chew, FS TI Peroneal nerve ganglion cyst SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 3 TC 8 Z9 8 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAR PY 1996 VL 166 IS 3 BP 682 EP 682 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TW774 UT WOS:A1996TW77400038 PM 8623650 ER PT J AU Wiener, DF Siliski, JM AF Wiener, DF Siliski, JM TI Distal femoral shaft fracture: A complication of endoscopic anterior cruciate ligament reconstruction - A case report SO AMERICAN JOURNAL OF SPORTS MEDICINE LA English DT Article ID SCREW HOLES RP Wiener, DF (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,15 PARKMAN ST WAC-525,BOSTON,MA 02114, USA. NR 19 TC 17 Z9 18 U1 0 U2 0 PU AMER ORTHOPAEDIC SOC SPORT MED PI WALTHAM PA 230 CALVARY STREET, WALTHAM, MA 02154 SN 0363-5465 J9 AM J SPORT MED JI Am. J. Sports Med. PD MAR-APR PY 1996 VL 24 IS 2 BP 244 EP 247 DI 10.1177/036354659602400224 PG 4 WC Orthopedics; Sport Sciences SC Orthopedics; Sport Sciences GA UA748 UT WOS:A1996UA74800024 PM 8775130 ER PT J AU Raines, DE AF Raines, DE TI Anesthetic and nonanesthetic halogenated volatile compounds wave dissimilar activities on nicotinic acetylcholine receptor desensitization kinetics SO ANESTHESIOLOGY LA English DT Article DE anesthetics, volatile, enflurane; isoflurane; nicotinic acetylcholine receptors, desensitization; theories, anesthetic action ID TORPEDO POSTSYNAPTIC MEMBRANES; GATED ION CHANNELS; GENERAL-ANESTHETICS; PRESSURE REVERSAL; FLUORESCENT AGONIST; BINDING; 30 mu g/g), prostate glands (>11 mu g/g), and lungs (>14 mu g/g). Plateau concentrations (2 to 8 h; given as mean micrograms per gram a standard error of the mean) of drug in kidneys (15.11 +/- 0.55), prostate glands (5.08 +/- 0.19), and lungs (5.75 +/- 0.22) were also well above the MIC(90) for most relevant pathogens. All patients had a good therapeutic response to fleroxacin. C1 MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. HARVARD MIT,DIV HLTH SCI & TECHNOL,CTR EXPTL PHARMACOL & THERAPEUT,CAMBRIDGE,MA. VET ADM OUTPATIENT CLIN,BOSTON,MA. BOSTON UNIV,SCH MED,BOSTON,MA 02118. W ROXBURY VET ADM HOSP,DEPT MED,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. RP Fischman, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 50 TC 21 Z9 22 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD MAR PY 1996 VL 40 IS 3 BP 659 EP 664 PG 6 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA TY366 UT WOS:A1996TY36600024 PM 8851589 ER PT J AU Paster, BJ Pelletier, DA Dewhirst, FE Weisburg, WG Fussing, V Poulsen, LK Dannenberg, S Schroeder, I AF Paster, BJ Pelletier, DA Dewhirst, FE Weisburg, WG Fussing, V Poulsen, LK Dannenberg, S Schroeder, I TI Phylogenetic position of the spirochetal genus Cristispira SO APPLIED AND ENVIRONMENTAL MICROBIOLOGY LA English DT Article ID RIBOSOMAL-RNA SEQUENCES; CELLS AB Comparative sequence analysis of 16S rRNA genes was used to determine the phylogenetic relationship of the genus Cristispira to other spirochetes. Since Cristispira organisms cannot presently be grown in vitro, 16S rRNA genes were amplified directly from bacterial DNA isolated from Cristispira a cell-laden crystalline styles of the oyster Crassostrea virginica. The amplified products were then cloned into Escherichia coli plasmids. Sequence comparisons of the gene coding for 16S rRNA (rDNA) insert of one clone, designated CP1, indicated that it was spirochetal. The sequence of the 16S rDNA insert of another clone was mycoplasmal. The CP1 sequence possessed most of the individual base signatures that are unique to 16S rRNA (or rDNA) sequences of known spirochetes. CP1 branched deeply among other spirochetal genera within the family Spirochaetaceae, and accordingly, it represents a separate genus within this family. A fluorescently labeled DNA probe designed from the CP1 sequence was used for in situ hybridization experiments to verify that the sequence obtained was derived from the observed Cristispira cells. C1 GENE TRAK SYST,FRAMINGHAM,MA 01701. DANISH VET LAB,DK-1790 COPENHAGEN V,DENMARK. TECH UNIV DENMARK,DEPT MICROBIOL,DK-2800 LYNGBY,DENMARK. UNIV CONSTANCE,DEPT MICROBIOL ECOL,W-7750 CONSTANCE,GERMANY. UNIV CALIF LOS ANGELES,DEPT MICROBIOL,LOS ANGELES,CA 90024. RP Paster, BJ (reprint author), FORSYTH DENT CTR,DEPT MOLEC GENET,140 FENWAY,BOSTON,MA 02115, USA. RI Pelletier, Dale/F-4154-2011 FU NIDCR NIH HHS [DE-10374, DE-08303] NR 32 TC 15 Z9 15 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0099-2240 J9 APPL ENVIRON MICROB JI Appl. Environ. Microbiol. PD MAR PY 1996 VL 62 IS 3 BP 942 EP 946 PG 5 WC Biotechnology & Applied Microbiology; Microbiology SC Biotechnology & Applied Microbiology; Microbiology GA TY365 UT WOS:A1996TY36500031 PM 8975621 ER PT J AU Sangueza, OP Galloway, J Eagan, PA Braziel, RM Gulley, ML AF Sangueza, OP Galloway, J Eagan, PA Braziel, RM Gulley, ML TI Absence of Epstein-Barr virus in lymphomatoid papulosis - An immunohistochemical and in situ hybridization study SO ARCHIVES OF DERMATOLOGY LA English DT Article ID T-CELL LYMPHOMA; HODGKINS-DISEASE; INSITU HYBRIDIZATION; NASOPHARYNGEAL CARCINOMA; MYCOSIS-FUNGOIDES; VIRAL GENOMES; DNA; INDIVIDUALS; EXPRESSION; ORIGIN AB Background and Design: Lymphomatoid papulosis (LyP) and cutaneous Hodgkin's disease share many clinical, histopathologic, and immunohistochemical features. Epstein-Barr virus (EBV) has been implicated in the pathogenesis of several lymphoid malignancies, including Hodgkin's disease. Given the similarities between LyP and Hodgkin's disease, we asked if EBV could be detected in lesions of LyP. We examined 31 specimens of LyP that were obtained from 24 patients for evidence of EBV by in situ hybridization to EBER1 transcripts and for immunohistochemistry of viral latent membrane protein 1 (LMP1). Results: In no instance was there any evidence of EBV gene products by either in situ hybridization or immunohistochemistry. Conclusions: The absence of EBV in LyP suggests that this virus is not operative in the pathogenesis of LyP. Furthermore, it suggests that LyP and Hodgkin's disease may not share the same molecular mechanisms despite their phenotypic similarities. C1 MED COLL GEORGIA,DEPT MED,DIV DERMATOL,AUGUSTA,GA 30912. OREGON HLTH SCI UNIV,DEPT PATHOL,PORTLAND,OR 97201. UNIV TEXAS,AUDIE L MURPHY MEM VET HOSP,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78285. RP Sangueza, OP (reprint author), MED COLL GEORGIA,DEPT PATHOL,1120 15TH ST,AUGUSTA,GA 30912, USA. FU NCI NIH HHS [CA01615] NR 44 TC 14 Z9 15 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD MAR PY 1996 VL 132 IS 3 BP 279 EP 282 DI 10.1001/archderm.132.3.279 PG 4 WC Dermatology SC Dermatology GA TZ573 UT WOS:A1996TZ57300005 PM 8607631 ER PT J AU McDonald, JA Potter, NU AF McDonald, JA Potter, NU TI Lead's Legacy? Early and late mortality of 454 lead-poisoned children SO ARCHIVES OF ENVIRONMENTAL HEALTH LA English DT Article ID SMELTER WORKERS; RENAL-FUNCTION; CHILDHOOD AB A series of 454 pediatric hospital patients who were diagnosed with lead poisoning between 1923 and 1966 were traced through 1991 to examine possible mortality effects. Numbers of observed deaths were compared with those expected, based on the rates of the U.S. population. Eighty-six deaths were observed (O/E = 1.7, 95% confidence interval (95% CI) = 1.4-2.2), of which 17 were attributed to lead poisoning. Mortality from all cardiovascular disease was elevated (O/E = 2.1, 95% CI = 1.3-3.2), and cerebrovascular deaths were particularly common among women (O/E = 5.5, 95% CI = 1.1-15.9). Among men, 2 deaths resulted from pancreatic cancer (O/E = 10.2, 95% CT = 1.1-36.2), and 2 deaths resulted from non-Hodgkin's lymphoma (O/E = 13.0, 95% Ci = 1.5-46.9). Chronic nephritis was not a significant cause of death. Despite limitations in the data, the pattern of mortality suggests that effects of lead poisoning in childhood may persist throughout life and may be experienced differently by men and women. C1 DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,BOSTON,MA 02115. UNIV VERMONT,DEPT MATH & STAT,BURLINGTON,VT 05405. NR 42 TC 12 Z9 13 U1 0 U2 0 PU HELDREF PUBLICATIONS PI WASHINGTON PA 1319 EIGHTEENTH ST NW, WASHINGTON, DC 20036-1802 SN 0003-9896 J9 ARCH ENVIRON HEALTH JI Arch. Environ. Health PD MAR-APR PY 1996 VL 51 IS 2 BP 116 EP 121 PG 6 WC Environmental Sciences; Public, Environmental & Occupational Health SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health GA UL917 UT WOS:A1996UL91700004 PM 8638961 ER PT J AU Dreyer, EB Zurakowski, D Schumer, RA Podos, SM Lipton, SA AF Dreyer, EB Zurakowski, D Schumer, RA Podos, SM Lipton, SA TI Elevated glutamate levels in the vitreous body of humans and monkeys with glaucoma SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID METHYL-D-ASPARTATE; RECEPTOR-MEDIATED NEUROTOXICITY; RETINAL GANGLION-CELLS; NMDA RECEPTORS; ANTAGONISTS; CULTURE AB Objective: To explore the possibility that the excitatory amino acid glutamate might be associated with the disease process of glaucoma, which is characterized by the death of retinal ganglion cell neurons and subsequent visual dysfunction. Methods: Amino acid analyses were performed on vitreous specimens that were obtained from patients who were undergoing cataract extraction. Samples were collected prospectively from those patients who sustained inadvertent rupture of the posterior capsule between 1988 and 1993. An additional set of specimens, obtained from both eyes of monkeys, was analyzed; in these monkeys, glaucoma had been experimentally induced in one eye only. Results: A twofold elevation in the level of glutamate was detected in the vitreous body of the group of patients with glaucoma when compared with that in a control population of patients with cataracts only. An even greater elevation of the glutamate level was found in the vitreous body of glaucomatous eyes of monkeys when compared with that in control eyes. No statistical differences were detected among other amino acid levels from the vitreous body of glaucomatous and nonglaucomatous eyes in humans or monkeys. Conclusions: The excitatory amino acid glutamate is found in the vitreous body of glaucomatous eyes at concentrations that are potentially toxic to retinal ganglion cells. The increased level of this known neurotoxin is consistent with an ''excitotoxic'' mechanism for the retinal ganglion cell and optic nerve damage in glaucoma. Therapies to protect neurons against glutamate toxic effects may prove to be useful in the management of this blinding disease. C1 HARVARD UNIV,CHILDRENS HOSP,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,DEPT RES COMP & BIOSTAT,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT NEUROL,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA. MT SINAI SCH MED,DEPT OPHTHALMOL,NEW YORK,NY. GLAXO CORP,RES TRIANGLE PK,NC. ALLERGAN PHARMACEUT INC,IRVINE,CA 92715. ALCON LABS INC,FT WORTH,TX 76101. PHARMOS CORP,ALACHUA,FL. RP Dreyer, EB (reprint author), MASSACHUSETTS EYE & EAR INFIRM,GLAUCOMA CONSULTAT SERV,243 CHARLES ST,BOSTON,MA 02114, USA. FU NEI NIH HHS [R01 EY10009, R01 EY05477] NR 41 TC 456 Z9 486 U1 2 U2 13 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD MAR PY 1996 VL 114 IS 3 BP 299 EP 305 PG 7 WC Ophthalmology SC Ophthalmology GA TZ301 UT WOS:A1996TZ30100010 PM 8600890 ER PT J AU Eavey, RD Pinto, LE Thornton, AR Herrmann, BS Bertero, MD Saenz, A AF Eavey, RD Pinto, LE Thornton, AR Herrmann, BS Bertero, MD Saenz, A TI Early hearing testing of still critically ill neonates SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Article ID BRAIN-STEM RESPONSE; INTENSIVE-CARE NURSERY; HIGH-RISK; AUDITORY-NERVE; FOLLOW-UP; EVOKED-RESPONSES; INFANTS; PRETERM; DEAFNESS; AUDIOMETRY AB Objective: To use a newly applied hearing screening technique for early measurement in neonatal intensive care unit (NICU) patients to learn more about the high incidence of hearing loss in this population. Methods: An automated, portable infant hearing screener that measures the auditory brain-stem response at the bedside was used at the NICU of the Hospital Nacional de Ninos, San Jose, Costa Rica. Patients were evaluated early, even if they were on a ventilator. The screener tested with a 40-dB hearing level click stimulus to each ear over a bandwidth of 750 to 3000 Hz. Results: During a 15-month period, 92 newborns underwent 226 auditory brain-stem response tests (range, one to six tests; mean, 21/2 tests). Before discharge from the NICU or death, each infant was successfully screened. Of 72 infants discharged from the hospital alive, 68 passed bilaterally and four failed bilaterally, a 6% failure rate. Of 20 infants who died, 15 failed bilaterally, a 75% failure rate. Persistent bilateral failure of the test was detectable from each infant's first test and showed an association (chi(2), P<.001) with death. The overall bilateral failure rate was 21%. Conclusions: Simple bedside auditory brain-stem response screening of all NICU infants was consistently possible regardless of clinical status, the early onset of hearing loss suggests that NICU treatment was not ototoxic, and the unexpectedly high overall bilateral test failure rate resulted from the inclusion of patients who would have died untested if conventional testing had been done. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. UNIV AUTONOMA CTR AMER,ESCUELA AUTONOMA CIENCIAS MED,DEPT PEDIAT,HOSP NACL NINOS,SAN JOSE,COSTA RICA. RP Eavey, RD (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 40 TC 2 Z9 2 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0886-4470 J9 ARCH OTOLARYNGOL JI Arch. Otolaryngol. Head Neck Surg. PD MAR PY 1996 VL 122 IS 3 BP 289 EP 293 PG 5 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA TZ300 UT WOS:A1996TZ30000011 PM 8607957 ER PT J AU Johnson, MW Washburn, WK Freeman, RB FitzMaurice, SE Dienstag, J Basgoz, N Jenkins, RL Cosimi, AB AF Johnson, MW Washburn, WK Freeman, RB FitzMaurice, SE Dienstag, J Basgoz, N Jenkins, RL Cosimi, AB TI Hepatitis C viral infection in liver transplantation SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 76th Annual Meeting of the New-England-Surgical-Society CY SEP 30-OCT 01, 1995 CL MONTREAL, CANADA SP New England Surg Soc ID NON-B-HEPATITIS; CHRONIC NON-A; POLYMERASE CHAIN-REACTION; RECIPIENTS; VIRUS; PREVALENCE; ANTIBODY; RNA AB Objective: To study the outcomes of patients who underwent liver transplantation for the primary diagnosis of chronic active hepatitis secondary to hepatitis C virus (HCV). Design and Setting: Retrospective review within a university medical center. Patients: Seventy-four adult recipients who received 78 orthotopic liver allografts for the primary diagnosis of chronic active hepatitis secondary to HCV between January 1990 and December 1994. Sixty-seven patients (91%) survived more than 2 months and were analyzed further for recurrent HCV infection. Main Outcome Measures: Recurrence of HCV infection, hepatitis, or cirrhosis and survival rates for patients who were undergoing orthotopic liver transplantation for chronic active hepatitis secondary to HCV. Results: Actuarial survival rates for the entire group were 79.3%, 70.9%, and 64.5% at 1, 2, and 3 years, respectively. Four patients (5%) underwent retransplantation with an actuarial survival rate of 14.3% at 1 year (P<.05). Thirty-eight patients (57%) had evidence of posttransplant HCV infection, 31 patients (46%) showed histologic evidence of viral hepatitis, and 11 patients (16%) experienced portal fibrosis or cirrhosis. Seven (33%) of the deaths and all retransplantations were secondary to recurrent HCV infection. There were no significant differences in age, sex, United Network of Organ Sharing status, associated diagnoses, intraoperative packed red blood cell requirements, OKT3 use, or 1-, 2-, and 3-year survival rates in the recurrent vs nonrecurrent HCV infection groups. A higher incidence of posttransplant cirrhosis was observed in patients who were treated with tacrolimus (FK 506) (31.8% vs 8.9%, P<.05). Twenty-one patients (70%) received interferon alfa antiviral therapy with a significant benefit in the liver function test results during therapy (P<.01). Conclusions: Despite recurrence of HCV infection in most patients after transplantation, survival following primary orthotopic liver transplantation for chronic active hepatititis secondary to HCV infection remains favorable, and these patients should continue to be candidates for liver transplantation. Tn contrast, survival following retransplantation for HCV infection is poor and should be reconsidered. There is an apparent association between the intensity of immunosuppression and recurrent HCV infection and cirrhosis that warrants continued evaluation. Interferon therapy appears to afford benefit to patients in whom recurrent HCV hepatitis develops after transplantation. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT INFECT DIS,BOSTON,MA 02114. NEW ENGLAND DEACONESS HOSP,HEPATOBILIARY UNIT,BOSTON,MA 02215. TUFTS UNIV NEW ENGLAND MED CTR,DIV TRANSPLANTAT,BOSTON,MA 02111. RI Washburn, William/Q-5677-2016 NR 26 TC 42 Z9 43 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD MAR PY 1996 VL 131 IS 3 BP 284 EP 291 PG 8 WC Surgery SC Surgery GA TZ297 UT WOS:A1996TZ29700019 PM 8611094 ER PT J AU Lipsitz, SR Parzen, M AF Lipsitz, SR Parzen, M TI A jackknife estimator of variance for cox regression for correlated survival data SO BIOMETRICS LA English DT Article DE clustered survival data; score vector AB Studies in the health sciences often give rise to correlated survival data. Wei, Lin, and Weissfeld (1989, Journal of the American Statistical Association 84, 1065-1073) and Lee, Wei, and Amato (1992, in Survival Analysis: State of the Art) showed that, if the marginal distributions of the correlated sur?rival times follow a proportional hazards model, then the estimates from Cox's partial likelihood (Cox, D. R., 1972, Journal of the Royal Statistical Society, Series B 24, 187-220), naively treating the correlated survival times as independent, give consistent estimates of the relative risk parameters. However, because of the correlation between survival times, the inverse of the information matrix may not be a consistent estimate of the asymptotic variance. Wei et al. (1989) and Lee et al. (1992) proposed a robust variance estimate that is consistent for the asymptotic variance. We show that a ''one-step'' jackknife estimator of variance is asymptotically equivalent to their variance estimator. The jackknife variance estimator may be preferred because an investigator needs only to write a simple loop in a computer package instead of a more involved program to compute Wei et al. (1989) and Lee et al.'s (1992) estimator. C1 DANA FARBER CANC INST, BOSTON, MA 02115 USA. UNIV CHICAGO, GRAD SCH BUSINESS, CHICAGO, IL 60637 USA. RP Lipsitz, SR (reprint author), HARVARD UNIV, SCH PUBL HLTH, DEPT BIOSTAT, 44 BINNEY ST, BOSTON, MA 02115 USA. FU NCI NIH HHS [CA 55576]; NIAID NIH HHS [AI 246431]; NIGMS NIH HHS [GM 29745] NR 7 TC 22 Z9 22 U1 0 U2 1 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 1996 VL 52 IS 1 BP 291 EP 298 DI 10.2307/2533164 PG 8 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA UF292 UT WOS:A1996UF29200026 PM 8934598 ER PT J AU Zhao, SC Ooi, SL Yang, FC Pardee, AB AF Zhao, SC Ooi, SL Yang, FC Pardee, AB TI Three methods for identification of true positive cloned cDNA fragments in differential display SO BIOTECHNIQUES LA English DT Article ID RNA RP Zhao, SC (reprint author), DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA61232] NR 9 TC 23 Z9 25 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD MAR PY 1996 VL 20 IS 3 BP 400 EP & PG 4 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TY801 UT WOS:A1996TY80100017 PM 8679198 ER PT J AU Manie, SN Astier, A Wang, DK Phifer, JS Chen, JC Lazarovits, AI Morimoto, C Freedman, AS AF Manie, SN Astier, A Wang, DK Phifer, JS Chen, JC Lazarovits, AI Morimoto, C Freedman, AS TI Stimulation of tyrosine phosphorylation after ligation of beta 7 and beta 1 integrins on human B cells SO BLOOD LA English DT Article ID FOCAL ADHESION KINASE; VLA-4; FIBRONECTIN; MOLECULE-1; IDENTIFICATION; ALPHA-4-BETA-7; EXPRESSION; SEQUENCES; BINDING AB B lymphocytes express several members of the integrin family of adhesion molecules that mediate cell-cell and cell-extracellular matrix interactions. In addition to beta 1 integrins, predominantly alpha 4 beta 1, mature B cells also express alpha 4 beta 7, which is a receptor for vascular cell adhesion molecule-1 and fibronectin, and is also involved in the homing of B cells to mucosal sites through binding to a third ligand. mucosal addressin cell adhesion molecule-1. Here we describe that crosslinking of alpha 4 beta 7 integrins on B cell lines and normal tonsillar B cells. induces tyrosine phosphorylation of multiple substrates of 105-130 kD, indicating that beta 7 integrin plays a role as signaling molecule in B cells. This pattern of phosphorylated proteins was very similar to that induced following ligation of alpha 4 beta 1. Interestingly, ligation of alpha 5 beta 1 or alpha 6 beta 1 also stimulated the 105-125 kD group of phosphorylated proteins, whereas ligation of beta 2 integrins did not. The focal adhesion tyrosine kinase p125(FAK) was identified as one of these substrates. beta 1 or beta 7 mediated tyrosine phosphorylations were markedly decreased when the microfilament assembly was inhibited by cytochalasin B. These results suggest that intracellular signals initiated by different integrins in B cells may converge, to similar cytoskeleton-dependent tyrosine phosphorylated proteins. (C) 1996 by The American Society of Hematology. C1 HARVARD UNIV,SCH MED,DEPT MED,DIV HEMATOL MALIGNANCIES,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT MED,DIV TUMOR IMMUNOL,BOSTON,MA. NEW ENGLAND DEACONESS HOSP,DANA FARBER CANC INST,DEPT HEMATOL ONCOL,BOSTON,MA 02215. UNIV WESTERN ONTARIO HOSP,JOHN P ROBARTS RES INST,LONDON,ON,CANADA. RI Astier, Anne/A-1641-2008 OI Astier, Anne/0000-0002-0144-3431 FU NCI NIH HHS [CA55207] NR 33 TC 38 Z9 38 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 1 PY 1996 VL 87 IS 5 BP 1855 EP 1861 PG 7 WC Hematology SC Hematology GA TY339 UT WOS:A1996TY33900024 PM 8634433 ER PT J AU Urashima, M Ogata, A Chauhan, D Hatziyanni, M Vidriales, MB Dedera, DA Schlossman, RL Anderson, KC AF Urashima, M Ogata, A Chauhan, D Hatziyanni, M Vidriales, MB Dedera, DA Schlossman, RL Anderson, KC TI Transforming growth factor-beta 1: Differential effects on multiple myeloma versus normal B cells SO BLOOD LA English DT Article ID NECROSIS-FACTOR-ALPHA; MARROW STROMAL CELLS; FACTOR-BETA; TGF-BETA; LYMPHOCYTES-B; INTERLEUKIN-6 PRODUCTION; AUTOCRINE INHIBITION; MESSENGER-RNAS; KILLER CELLS; IN-VITRO AB Interleukin-6 (IL-6), a product of bone marrow stromal cells (BMSCs), is a growth factor for multiple myeloma (NIM) cells. Transforming growth factor-beta 1 (TGF-beta 1) is also produced by BMSCs and can regulate IL-6 secretion by several tissues, including BMSCs. The present study was designed to characterize in vitro tumor growth regulation by TGF-beta 1 in MM. Sorted CD38(+)CD45RA(-) MM cells secreted significantly more TGF-beta 1 (8.2 +/- 2.0 ng/mL) than peripheral blood mononuclear cells (P < .001), splenic B cells (P < .001), and CD40 ligand (CD40L) pretreated B cells (P < .05). TGF-beta 1 secretion by MM-BMMCs (3.8 +/- 0.9 ng/mL) was significantly greater than by N-BMMCs (1.2 +/- 0.1 ng/mL P < .001). MM-BMSCs also secreted significantly more TGF-beta 1 (6.6 +/- 2.5 ng/mL, n = 11) than N-BMSCs (4.4 +/- 0.6 ng/mL, P < .02, n = 10) and N-BMSC lines (3.9 +/- 0.2 ng/mL, P < .02, n = 6). TGF-beta 1 secretion was correlated with IL-6 secretion in MM-BMSCs. Anti-TGF-beta 1 monoclonal antibody both blocked IL-6 secretion by BMSCs and inhibited the increments in IL-6 secretion by BMSCs induced by MM cell adhesion. Moreover, exogenous TGF-beta 1 upregulated IL-6 secretion by MM-BMSCs, normal BMSCs, and CD38(+) CD45RA(-) MM cells, as well as tumor cell proliferation. This is in contrast to the inhibitory effect of TGF-beta 1 on proliferation and Ig secretion of normal splenic B cells. Finally, retinoblastoma proteins (pRB) are constitutively phosphorylated in MM cells; TGF-beta 1 either did not alter or increased pRB phosphorylation. pRB are dephosphorylated in splenic B cells and phosphorylated in CD40L triggered B cells; in contrast to its effects on MM cells, TGF-beta 1 decreased phosphorylation of pRB in CD40L treated B cells. These results suggest that TGF-beta 1 is produced in MM by both tumor cells and BMSCs and can trigger IL-6 secretion by both MM cells and BMSCs, with related tumor cell growth. Moreover, MM cell growth may be enhanced by resistance of tumor cells to the inhibitory effects of TGF-beta 1 on normal B-cell proliferation and Ig secretion. (C) 1996 by The American Society of Hematology. C1 DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. RI Vidriales, Maria-Belen/L-1277-2013; OI Vidriales, Maria-Belen/0000-0001-5049-3673 FU NCI NIH HHS [CA50947] NR 70 TC 161 Z9 172 U1 0 U2 5 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 1 PY 1996 VL 87 IS 5 BP 1928 EP 1938 PG 11 WC Hematology SC Hematology GA TY339 UT WOS:A1996TY33900032 PM 8634441 ER PT J AU Emoto, Y Kisaki, H Manome, Y Kharbanda, S Kufe, D AF Emoto, Y Kisaki, H Manome, Y Kharbanda, S Kufe, D TI Activation of protein kinase C delta in human myeloid leukemia cells treated with 1-beta-D-arabinofuranosylcytosine SO BLOOD LA English DT Article ID INTERNUCLEOSOMAL DNA FRAGMENTATION; JUN GENE-EXPRESSION; POTENTIAL INVOLVEMENT; TRANSCRIPTION FACTOR; PHORBOL ESTER; KAPPA-B; PHOSPHORYLATION; ARABINOFURANOSYLCYTOSINE; INHIBITORS; MECHANISM AB Treatment of human myeloid leukemia cells with 1-beta-D-arabinofuranosylcytosine (ara-C) is associated with induction of protein kinase activity and early-response gene expression. The present studies in ara-C-treated U-937 cells extend these findings by demonstrating activation of a protein kinase that phosphorylates myelin basic protein (MBP), Purification by sequential ion-exchange chromatography and gel filtration supports the detection of a 40-kD MBP kinase. Substrate and inhibitor studies further support a pattern similar to that of protein kinase C (PKC) isozymes, Results of N-terminal amino acid sequencing and immunoblot analysis demonstrate detection of a 40-kD catalytic fragment of PKC delta. The results also demonstrate that activation and cleavage of PKC delta (1) is inhibited by expression of antiapoptotic proteins, and (2) is induced by camptothecin (CAM) and mitomycin C (MMC), These findings support proteolytic activation of PKC delta in the cellular response to ara-C and other DNA-damaging agents. (C) 1996 by The American Society of Hematology. RP Emoto, Y (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA29431] NR 48 TC 116 Z9 118 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 1 PY 1996 VL 87 IS 5 BP 1990 EP 1996 PG 7 WC Hematology SC Hematology GA TY339 UT WOS:A1996TY33900040 PM 8634449 ER PT J AU Stromswold, K Caplan, D Alpert, N Rauch, S AF Stromswold, K Caplan, D Alpert, N Rauch, S TI Localization of syntactic comprehension by positron emission tomography SO BRAIN AND LANGUAGE LA English DT Article ID WORKING MEMORY; SENTENCE COMPREHENSION; INDIVIDUAL-DIFFERENCES; BRAIN POTENTIALS; APHASIA; LANGUAGE; DISSOCIATION; NETWORKS; RECOVERY; STIMULI AB Positron Emission Tomography (PET) was used to determine regional cerebral blood flow (rCBF) when eight normal right-handed males read and made acceptability judgments about sentences. rCBF was greater in Broca's area (particularly in the pars opercularis) when subjects judged the semantic plausibility of syntactically more complex sentences as compared to syntactically less complex sentences. rCBF was greater in left perisylvian language areas when subjects had to decide whether sentences were semantically plausible than when subjects had to decide whether syntactically identical sentences contained a nonsense word. The results of this experiment suggest that overall sentence processing occurs in regions of the left perisylvian association cortex. The results also provide evidence that one particular aspect of sentence processing (the process that corresponds to the greater difficulty of comprehending center-embedded than right-branching relative clause sentences) is centered in the pars opercularis of Broca's area. This process is likely to be related to the greater memory load associated with processing center-embedded sentences. (C) 1996 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP, NEUROPSYCHOL LAB, DEPT NEUROL, BOSTON, MA 02114 USA. MIT, DEPT BRAIN & COGNIT SCI, CAMBRIDGE, MA 02139 USA. MASSACHUSETTS GEN HOSP, DEPT RADIOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PSYCHIAT, BOSTON, MA 02114 USA. FU NCI NIH HHS [T32CAO93262]; NIDCD NIH HHS [1RO3-DC01198, IRO3-DC01198] NR 55 TC 409 Z9 415 U1 1 U2 9 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0093-934X EI 1090-2155 J9 BRAIN LANG JI Brain Lang. PD MAR PY 1996 VL 52 IS 3 BP 452 EP 473 DI 10.1006/brln.1996.0024 PG 22 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA UC242 UT WOS:A1996UC24200003 PM 8653390 ER PT J AU Dalmas, S Marsch, SCU Philbin, DM Gavaghan, DJ Ryder, WA Foex, P AF Dalmas, S Marsch, SCU Philbin, DM Gavaghan, DJ Ryder, WA Foex, P TI Effects and interactions of myocardial ischaemia and alterations in circulating blood volume on canine left ventricular diastolic function SO BRITISH JOURNAL OF ANAESTHESIA LA English DT Article DE heart, ischaemia; heart, myocardial function; heart, ventricles; blood, volume; dog ID CORONARY-ARTERY DISEASE; HEMODYNAMIC DETERMINANTS; ISOVOLUMIC RELAXATION; INDUCED ISCHEMIA; CONSCIOUS DOG; TIME-COURSE; PRESSURE; HEART; PRELOAD; HUMANS AB We have determined the effects of alterations in preload on ischaemia-induced diastolic dysfunction in anaesthetized beagles instrumented to measure left ventricular pressure and regional dimensions. ischaemia decreased peak in ischaemic (mean -26 (SEM 6) mm s(-1), P < 0.01) and non-ischaemic (-8.6 (3.4) mm s(-1), P < 0.05) myocardium. Peak lengthening rates and the time constant of isovolumic relaxation (tau) were not affected by alterations in preload. Absolute values of tau failed to distinguish between ischaemia and control. The ischaemia-induced decrease in peak negative dP/dt was preload dependent and caused mainly by a concomitant decrease in peak left ventricular pressure. We conclude that indices derived from segmental lengthening are sensitive to ischaemia and insensitive to preload, in contrast with indices derived from left ventricular pressure. It remains to be determined if monitoring of early segmental lengthening will improve detection and assessment of perioperative myocardial ischaemia. C1 RADCLIFFE INFIRM,NUFFIELD DEPT ANAESTHET,OXFORD OX2 6HE,ENGLAND. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. OI gavaghan, david/0000-0001-8311-3200 FU Wellcome Trust NR 33 TC 4 Z9 4 U1 0 U2 0 PU PROF SCI PUBL PI LONDON PA TAVISTOCK HOUSE EAST, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-0912 J9 BRIT J ANAESTH JI Br. J. Anaesth. PD MAR PY 1996 VL 76 IS 3 BP 419 EP 427 PG 9 WC Anesthesiology SC Anesthesiology GA TW746 UT WOS:A1996TW74600017 PM 8785145 ER PT J AU Schmidt, AM Crandall, J Hori, O Cao, R Lakatta, E AF Schmidt, AM Crandall, J Hori, O Cao, R Lakatta, E TI Elevated plasma levels of vascular cell adhesion molecule-1 (VCAM-1) in diabetic patients with microalbuminuria: A marker of vascular dysfunction and progressive vascular disease SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article DE glycation; diabetes; adhesion molecule; microalbuminuria; vasculopathy ID MELLITUS; ALBUMIN AB Advanced glycation endproducts (AGEs), which accumulate in diabetic vasculature, result in enhanced expression of endothelial cell-associated vascular cell adhesion molecule-1 (VCAM-1) as well release of a soluble form of VCAM-1 (sVCAM-1) into culture supernatants. We hypothesized that sVCAM-1 in diabetic plasma might reflect early vascular perturbation in diabetic vasculopathy. Diabetic patients with microalbuminuria, a group with a high incidence of vascular complications, had increased plasma levels of sVCAM-1, similar to 1.5-fold greater than diabetic patients without microalbuminuria: P<0.05. sVCAM-1 map be an indicator of ongoing cellular dysfunction in diabetes, as well as a dynamic surrogate marker for the effectiveness of therapeutic interventions. C1 COLUMBIA UNIV COLL PHYS & SURG,DEPT SURG,NEW YORK,NY 10032. COLUMBIA UNIV COLL PHYS & SURG,DEPT PHYSIOL,NEW YORK,NY 10032. ST LUKES ROOSEVELT HOSP,DEPT MED,JOSLIN DIABET CTR,NEW YORK,NY 10025. NIA,GERONTOL RES CTR,CARDIOVASC RES LAB,BALTIMORE,MD. RP Schmidt, AM (reprint author), COLUMBIA UNIV COLL PHYS & SURG,DEPT MED,630 W 168TH ST,P&S 11-518,NEW YORK,NY 10032, USA. FU NHLBI NIH HHS [HL 21006, HL 42507]; NIA NIH HHS [AG00602] NR 12 TC 85 Z9 87 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD MAR PY 1996 VL 92 IS 3 BP 747 EP 750 DI 10.1046/j.1365-2141.1996.379915.x PG 4 WC Hematology SC Hematology GA TY265 UT WOS:A1996TY26500039 PM 8616048 ER PT J AU Sasson, S Gorowits, N Joost, HG King, GL Cerasi, E Kaiser, N AF Sasson, S Gorowits, N Joost, HG King, GL Cerasi, E Kaiser, N TI Regulation by metformin of the hexose transport system in vascular endothelial and smooth muscle cells SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE metformin; glucose transporter; vascular endothelium; vascular smooth muscle; diabetes mellitus; non-insulin dependent; hexose transport ID GLUCOSE-TRANSPORT; INTRACELLULAR POOL; PLASMA-MEMBRANE; SKELETAL-MUSCLE; INSULIN; CULTURE; TRANSLOCATION; STIMULATION; ADIPOCYTES; METABOLISM AB 1 The effect of the biguanide metformin on hexose transport activity was studied in bovine cultured aortic endothelial (BEG) and smooth muscle cells (BSMC). 2 Metformin elevated the rate of hexose transport determined with, 2-deoxyglucose (2DG) in a dose- and time-dependent manner in both cell types. Similar ED(50) values (0.8-1.0 mM) were determined for the effect of metformin on 2DG uptake in both BEC and BSMC following 24 h exposure to increasing concentrations of metformin, with maximal stimulation at 2 mM. 3 In BEG, metformin increased the hexose transport rate 2-3 fold at all glucose concentrations tested (3.3-22.2 mM). In BSMC incubated with 22.2 mM glucose, metformin elevated the hexose transport similar to 2 fold. The drug was also effective at lower glucose levels, but did not exceed the maximal transport rate observed in glucose-deprived cells. 4 Similar results were obtained when the effect of metformin on hexose transport activity was assessed with the non-metabolizable hexose analogue, 3-O-methylglucose, suggesting that the drug affects primarily the rate of hexose transport rather than its subsequent phosphorylation. 5 The metformin-induced increase in hexose transport in BSMC treated for 24 h with the drug correlated with increased abundance of GLUT1 protein in the plasma membrane, as determined by Western blot analysis. 6 These data indicate that in addition to its known effects on hexose metabolism in insulin responsive tissues, metformin also affects the hexose transport system in vascular cells. This may contribute to its blood glucose lowering capacity in patients with Type 2, non-insulin-dependent diabetes mellitus. C1 HEBREW UNIV JERUSALEM,SCH MED,SCH PHARM,DEPT PHARMACOL,IL-91010 JERUSALEM,ISRAEL. HEBREW UNIV JERUSALEM,HADASSAH MED CTR,DEPT ENDOCRINOL & METAB,JERUSALEM,ISRAEL. RHEIN WESTFAL TH AACHEN,INST PHARMAKOL & TOXIKOL,W-5100 AACHEN,GERMANY. JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. RI Joost, Hans-Georg/J-4462-2013 OI Joost, Hans-Georg/0000-0002-5860-606X NR 33 TC 15 Z9 18 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD MAR PY 1996 VL 117 IS 6 BP 1318 EP 1324 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA UB816 UT WOS:A1996UB81600045 PM 8882631 ER PT J AU Rosenbaum, JF Pollock, RA Jordan, SK Pollack, MH AF Rosenbaum, JF Pollock, RA Jordan, SK Pollack, MH TI The pharmacotherapy of panic disorder SO BULLETIN OF THE MENNINGER CLINIC LA English DT Article; Proceedings Paper CT Menninger Symposium on Panic Disorder Update - Cost, Comorbidity, Outcomes, at the Annual Meeting of the American-Psychiatric-Association CY MAY 04-08, 1996 CL NEW YORK, NY SP Amer Psychiat Assoc ID MAINTENANCE DRUG-TREATMENT; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; ANXIETY DISORDERS; FOLLOW-UP; BENZODIAZEPINE TREATMENT; BEHAVIORAL-INHIBITION; SHORT-TERM; GENERALIZED ANXIETY; SOCIAL PHOBIA AB The biological model for panic disorder posits a specific, genetically inherent neurochemical dysfunction; pharmacological treatment attempts to reregulate the dysregulated physiological system, thereby achieving remission (or, ideally, recovery) or amelioration of the symptoms sufficient for nonpharmacological therapies to be viable. This article will review the evidence of the efficacy of single classes of pharmacological agents (antidepressants, including TCAs, MAOIs, and SSRIs; benzodiazepines; and other agents) and integrated treatments, involving coadministration of medications within or across classes or a combination of pharmacological and nonpharmacological therapies, such as cognitive-behavioral therapy. Research pertaining to the relative efficacy of administering combination treatments concurrently or sequentially is examined. Individualized treatment plans for patients maximize the benefits of integrated treatments. C1 MASSACHUSETTS GEN HOSP,OUTPATIENT PSYCHIAT DIV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,ANXIETY DISORDERS RES PROGRAM,BOSTON,MA 02114. RP Rosenbaum, JF (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,WAC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 117 TC 6 Z9 6 U1 3 U2 4 PU MENNINGER FOUNDATION PI TOPEKA PA BOX 829, TOPEKA, KS 66601 SN 0025-9284 J9 B MENNINGER CLIN JI Bull. Menninger Clin. PD SPR PY 1996 VL 60 IS 2 SU A BP A54 EP A75 PG 22 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA UN009 UT WOS:A1996UN00900005 PM 8857427 ER PT J AU Mangham, DC Cannon, A Komiya, S Gendron, RL Dunussi, K Gebhardt, MC Mankin, HJ Arceci, RJ AF Mangham, DC Cannon, A Komiya, S Gendron, RL Dunussi, K Gebhardt, MC Mankin, HJ Arceci, RJ TI P-glycoprotein is expressed in the mineralizing regions of the skeleton SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article DE P-glycoprotein; growth plate; cartilage; bone ID MULTIDRUG-RESISTANCE GENE; MONOCLONAL-ANTIBODIES; DRUG ACCUMULATION; HUMAN-TISSUES; CELLS; MDR1; CYCLOSPORINE; ASSOCIATION; TRANSPORT; DISEASE AB Using oligonucleotide primers specific for the human MDR 1 gene, we were able to identify a specific amplicon using RT-PCR from total bovine growth plate chondrocyte RNA. The identification of MDR mRNA in growth plate chondrocytes led us to examine the precise distribution of MDR P-glycoprotein in bone and cartilage. We applied two monoclonal antibodies (C219 and C494) to human fetal, neonatal, and childhood growth plates and bone. In growth plates, P-glycoprotein was detected at high levels in a perilacunar distribution in the calcifying zone and at lower levels in hypertrophic, but not proliferative or reserve zone, chondrocytes. P-glycoprotein was also observed in perichondrial chondrocytes, in perivascular chondrocytes and matrix in the fetal cartilage anlage, and in osteoblasts and the surface osteoid matrix of newly formed bone trabeculae in the primary spongiosa. The recently described chloride channel of P-glycoprotein suggests a potential role of P-glycoprotein in growth plate chondrocyte hypertrophy. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED RES LABS,BOSTON,MA 02114. CHILDRENS HOSP,DEPT PEDIAT HEMATOL & ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 29 TC 13 Z9 13 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD MAR PY 1996 VL 58 IS 3 BP 186 EP 191 DI 10.1007/BF02526885 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA TY392 UT WOS:A1996TY39200011 PM 8852574 ER PT J AU Rainov, NG Kramm, CM AboodyGuterman, K Chase, M Ueki, K Louis, DN Harsh, GR Chiocca, A Breakefield, XO AF Rainov, NG Kramm, CM AboodyGuterman, K Chase, M Ueki, K Louis, DN Harsh, GR Chiocca, A Breakefield, XO TI Retrovirus-mediated gene therapy of experimental brain neoplasms using the herpes simplex viruus thymidine kinase ganciclovir paradigm SO CANCER GENE THERAPY LA English DT Article DE brain neoplasms; herpes simplex virus; thymidine kinase; ganciclovir ID GLIOMA-CELLS; TUMOR-CELLS; RAT-BRAIN; INVIVO; BEARING; VECTORS; INSITU; MODEL; LINE AB Recent results in experimental brain tumors indicate that transfer of sensitizing genes to tumor cells in vivo with subsequent drug treatment can reduce tumor masses and prolong the survival of rodents. In the present study, the 9L rat gliosarcoma model was used to evaluate the therapeutic effectiveness of the herpes simplex virus-thymidine kinase (HSV-tk) gene, delivered by a retrovirus vector, against tumor cells in the rat brain after systemic application of the nucleoside analogue ganciclovir (GCV). The HSV-tk gene was inserted into a retroviral vector (pMFG), which was produced using the amphotropic packaging cell line CRIP-MFG-S-HSV-TK. Packaging cells were implanted into established 9L rumors in the brains of syngeneic rats to effect gene delivery to tumor cells, followed by intraperitoneal GCV injections. Treated animals survived significantly longer (more than twice as long) than did the control groups. Brains from GCV-treated and nontreated animals were examined immunohistochemically at different time intervals after grafting of CRIP-MFG-S-HSV-TK cells and GCV treatment. Tumors in GCV-treated animals were significantly smaller as compared with nontreated animals at all time points. Sections stained immunohistochemically for HSV-TK confirmed gene transfer to tumor cells, which could be distinguished from packaging cells by different morphology and immunohistochemical staining for the retroviral envelope protein gp70. Approximately 45% of the cells in tumors implanted with CRIP-MFG-S-HSV-TK cells, but not treated with GCV, showed immunocytochemical staining for HSV-TK, demonstrating a high-efficiency of retrovirus-mediated gene transfer. Tumors in rats treated with packaging cells and GCV showed only 9% HSV-TK-positive cells after treatment, indicating that most cells expressing the HSV-tk gene were killed. The success of this therapeutic modality in experimental animals depends in large parts on the high efficiency of gene delivery and on the immune response against tumor cells. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. UNIV HALLE WITTENBERG,FAC MED,DEPT NEUROSURG,HALLE,GERMANY. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. FU NINDS NIH HHS [NS24279] NR 43 TC 45 Z9 45 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0929-1903 J9 CANCER GENE THER JI Cancer Gene Ther. PD MAR-APR PY 1996 VL 3 IS 2 BP 99 EP 106 PG 8 WC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity; Research & Experimental Medicine GA UE286 UT WOS:A1996UE28600004 PM 8729908 ER PT J AU Huang, L Son, K Gao, X Hages, D Yang, YY Holden, SA Teicher, B Kirkwood, J Lazo, JS AF Huang, L Son, K Gao, X Hages, D Yang, YY Holden, SA Teicher, B Kirkwood, J Lazo, JS TI Efficient lipofection with cisplatin-resistant human tumor cells SO CANCER GENE THERAPY LA English DT Article DE lipofection; cisplatin; drug resistance; gene therapy ID OVARIAN-CARCINOMA CELLS; SUBLINES RESISTANT; CATIONIC LIPOSOMES; MAMMALIAN-CELLS; RNA-POLYMERASE; LEUKEMIA-CELLS; CIS-DIAMMINEDICHLOROPLATINUM(II); EXPRESSION; GENE; DNA AB Seven of seven different cisplatin-resistant human tumor cell lines showed elevated lipofection activity as compared with their sensitive parent cells, although the degree of enhancement was not quantitatively correlated with the degree of cisplatin resistance. Enhanced transfection was seen by using the same reporter gene driven by three different promoter/enhancer sequencer or by using different reporter genes driven by the same promoter/enhancer. Cells resistant to actinomycin D, bleomycin, and nitrogen mustards were not more transfectable than the sensitive parent cells. Although the mechanism of enhanced transfection in cisplatin-resistant cells is not known, data indicated that enhanced transcription, multidrug-resistant phenotype, and methallothionein overexpression do not play a role. C1 UNIV PITTSBURGH,SCH MED,DEPT MED,PITTSBURGH,PA 15261. DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. RP Huang, L (reprint author), UNIV PITTSBURGH,SCH MED,DEPT PHARMACOL,W1351 BIOMED SCI TOWER,PITTSBURGH,PA 15261, USA. FU NCI NIH HHS [CA38493, CA59327, CA61299] NR 32 TC 6 Z9 6 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0929-1903 J9 CANCER GENE THER JI Cancer Gene Ther. PD MAR-APR PY 1996 VL 3 IS 2 BP 107 EP 112 PG 6 WC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Oncology; Genetics & Heredity; Research & Experimental Medicine GA UE286 UT WOS:A1996UE28600005 PM 8729909 ER PT J AU Znati, CA Rosenstein, M Boucher, Y Epperly, MW Bloomer, WD Jain, RK AF Znati, CA Rosenstein, M Boucher, Y Epperly, MW Bloomer, WD Jain, RK TI Effect of radiation on interstitial fluid pressure and oxygenation in a human tumor xenograft SO CANCER RESEARCH LA English DT Article ID MONOCLONAL-ANTIBODY UPTAKE; BLOOD-FLOW; HYPERTENSION; IRRADIATION; ENHANCEMENT; CARCINOMA AB Elevated interstitial fluid pressure (IFP) is a pathophysiological characteristic of most human and experimental tumors and may be responsible, in part, for the poor distribution of blood-borne therapeutic agents and low blood flow rate in tumors. Recent data in cervical carcinomas in patients suggest that fractionated radiation can lower tumor IFP and increase oxygen partial pressure (pO(2)) in some patients. The goals of this study were to find the minimum dose of radiation required to modulate IFP and pO(2) and to determine the time course of IFP changes due to radiation in a preclinical model. Xenografts of the LS174T human colon adenocarcinoma were grown in the right flank of nude (BALB/c) mice. IFP and pO(2) were measured before and 24 h after graded doses of irradiation. The mean +/- SD initial IFP in untreated tumors was 12.9 +/- 0.5 mm Hg (n = 109), and the range was 3.0 to 40.3 mm Hg. The mean +/- SD and median initial pO(2) were 20.2 +/- 2.4 and 11.9 mm Hg, respectively (n = 37). IFP and pO(2) were independent of tumor size. Fractionated radiation lowered IFP by 2.5 mm Hg when the total dose was 10 or 15 Gy (P < 0.05), but IFP did not change in the controls or the 5-Gy radiation group (P > 0.05). Irradiation increased the proportion of tumors at higher oxygen tensions n hen compared to control tumors. The IFP and tumor volumes were followed for up to 10 days after a single dose of 10, 20, or 30 Gy of irradiation. IFP decreased for all treatment groups. The decrease was most significant for the group receiving 30 Gy. On day five following irradiation, the IFP had decreased by 35%. The changes in IFP and pO(2) occurred before any macroscopic changes in tumor volume could be observed. The radiation-induced decrease in IFP could be, in part, responsible for the increased uptake of monoclonal antibodies following single or fractionated radiation that has been reported in the literature. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. CARNEGIE MELLON UNIV,DEPT CHEM ENGN,PITTSBURGH,PA 15213. UNIV PITTSBURGH,DEPT RADIAT ONCOL,PITTSBURGH,PA 15213. EVANSTON HOSP CORP,DEPT RADIAT MED,EVANSTON,IL 60201. FU NCI NIH HHS [R35-CA-56591] NR 29 TC 92 Z9 93 U1 0 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 1 PY 1996 VL 56 IS 5 BP 964 EP 968 PG 5 WC Oncology SC Oncology GA TX173 UT WOS:A1996TX17300008 PM 8640786 ER PT J AU Molpus, KL Kato, D Hamblin, MR Lilge, L Bamberg, M Hasan, T AF Molpus, KL Kato, D Hamblin, MR Lilge, L Bamberg, M Hasan, T TI Intraperitoneal photodynamic therapy of human epithelial ovarian carcinomatosis in a xenograft murine model SO CANCER RESEARCH LA English DT Article ID TUMOR-NECROSIS-FACTOR; BEARING MICE; PHASE-I; MACROPHAGES; SHOCK; PHOTOSENSITIZERS; HEMATOPORPHYRIN; MECHANISMS; ENDOTOXIN; CACHECTIN AB The objective of this investigation was to determine the efficacy of i.p. photodynamic therapy (PDT) against solid, multifocal ovarian carcinoma using a newly described NIH:OVCAR-5 induced murine model, PDT was initiated when diffuse microscopic disease and small multifocal tumor nodules were present, similar to the extent of residual carcinoma that may persist clinically after laparotomy and tumor debulking, The photosensitizer, benzoporphyrin derivative monoacid ring A (BPD-MA), was administered in a dose of 0.25 mg/kg body weight i.p. 90 min prior to light exposure, An argon-pumped dye laser was used to deliver low intensity light (20 J) i.p. through a cylindrically diffusing fiberoptic tip, Treatment regimens consisted of a series of three to five treatments at 3-7-day intervals, with the extent of macroscopic disease or death from disease being the evaluable outcome parameters for tumoricidal and survival studies, respectively, The mean tumor burden at necropsy for treated animals was 0.034 +/- 0.014 g compared to 0.379 +/- 0.065 g in untreated controls (P < 0.001), Survival studies were initiated in two groups at day 7 and day 14 following cell inoculation, The first group received either three or five treatments at 5-day intervals, and both had a significant increase in median survival compared to untreated controls (57 and 53 days, respectively, compared to 43 days, P < 0.05), The second group was treated every 7 days until death and also had a significant survival advantage over controls (57 days compared to 47 days, P < 0.05), These studies suggest that benzoporphyrin derivative mono acid ring A-mediated PDT is a feasible, well-tolerated, experimental treatment approach that elicits a tumoricidal response against diffuse, solid i.p. disease in tumor-bearing mice, with concomitant prolongation of survival and needs careful optimization. C1 MASSACHUSETTS GEN HOSP, WELLMAN LABS PHOTOMED, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, VINCENT GYNECOL ONCOL SERV, BOSTON, MA 02114 USA. PRINCESS MARGARET HOSP, ONTARIO CANC INST, DEPT CLIN PHYS, TORONTO, ON M5G 2M6, CANADA. RI Lilge, lothar/J-6434-2013; OI Hamblin, Michael/0000-0001-6431-4605 FU NIAMS NIH HHS [R01 AR40352] NR 53 TC 49 Z9 52 U1 2 U2 4 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 1 PY 1996 VL 56 IS 5 BP 1075 EP 1082 PG 8 WC Oncology SC Oncology GA TX173 UT WOS:A1996TX17300025 PM 8640764 ER PT J AU Duerinckx, AJ Lewis, BS Louie, HW Urman, MK AF Duerinckx, AJ Lewis, BS Louie, HW Urman, MK TI MRI of pseudoaneurysm of a brachial venous coronary bypass graft SO CATHETERIZATION AND CARDIOVASCULAR DIAGNOSIS LA English DT Article DE MR imaging; coronary bypass graft; pseudoaneurysm ID SAPHENOUS-VEIN GRAFT; ANGIOGRAPHY; ARTERIES; PATENCY AB Coronary artery bypass grafting (CABG) is being performed all over the world, with major success in the management of ischemic heart disease and angina pectoris, Complications of bypass grafting include partial or total graft reocclusion, and less common entities such as aneurysm or pseudoaneurysm formation, Noninvasive imaging procedures exist which can help include or exclude the presence of these unusual types of complications when mass-like abnormalities are seen on a chest X-ray following coronary artery bypass grafting. This case specifically illustrates the usefulness of ultrafast magnetic resonance imaging techniques in the evaluation and diagnosis of pseudoaneurysm formation at the site of coronary artery bypass graft. (C) 1996 Wiley-Liss, Inc. C1 UNIV CALIF LOS ANGELES,MED CTR,DEPT CARDIOTHORAC SURG,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,MED CTR,DEPT RADIOL,LOS ANGELES,CA 90024. CEDARS SINAI MED TOWERS,LOS ANGELES,CA. RP Duerinckx, AJ (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,SERV RADIOL,MAIL ROUTE W114,MRI,BLD 507,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 26 TC 4 Z9 4 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0098-6569 J9 CATHETER CARDIO DIAG JI Catheter. Cardiovasc. Diagn. PD MAR PY 1996 VL 37 IS 3 BP 281 EP 286 DI 10.1002/(SICI)1097-0304(199603)37:3<281::AID-CCD14>3.0.CO;2-L PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA TX726 UT WOS:A1996TX72600014 PM 8974807 ER PT J AU Dinsmore, J Ratliff, J Deacon, T Pakzaban, P Jacoby, D Galpern, W Isacson, O AF Dinsmore, J Ratliff, J Deacon, T Pakzaban, P Jacoby, D Galpern, W Isacson, O TI Embryonic stem cells differentiated in vitro as a novel source of cells for transplantation SO CELL TRANSPLANTATION LA English DT Article; Proceedings Paper CT 2nd Annual Meeting of the American-Society-for-Neural-Transplantation CY APR 27-29, 1995 CL CLEARWATER, FL SP Amer Soc Neural Transplantat DE stem cells; differentiation; GABAergic neurons; transplantation ID LEUKEMIA INHIBITORY FACTOR; NERVE GROWTH-FACTOR; GERM-LINE CHIMERAS; ES CELLS; NEURONAL DIFFERENTIATION; MOUSE; CULTURE; INVITRO; EXPRESSION; PROLIFERATION AB The controlled differentiation of mouse embryonic stem (ES) cells into near homogeneous populations of both neurons and skeletal muscle cells that can survive and function in vivo after transplantation is reported, We show that treatment of pluripotent ES cells with retinoic acid (RA) and dimethylsulfoxide (DMSO) induce differentiation of these cells into highly enriched populations of gamma-aminobutyric acid (GABA) expressing neurons and skeletal myoblasts, respectively. For neuronal differentiation, RA alone is sufficient to induce ES cells to differentiate into neuronal cells that show properties of postmitotic neurons both in vitro and in vivo, In vivo function of RA-induced neuronal cells was demonstrated by transplantation into the quinolinic acid lesioned striatum of rats (a rat model for Huntington's disease), where cells integrated and survived for up to 6 wk, The response of embryonic stem cells to DMSO to form muscle was less dramatic than that observed for RA, DMSO-induced ES cells formed mixed populations of muscle cells composed of cardiac, smooth, and skeletal muscle instead of homogeneous populations of a single muscle cell type, To determine whether the response of ES cells to DMSO induction could be further controlled, ES cells were stably transfected with a gene coding for the muscle-specific regulatory factor, MyoD, When induced with DMSO, ES cells constitutively expressing high levels of MyoD differentiated exclusively into skeletal myoblasts (no cardiac or smooth muscle cells) that fused to form myotubes capable of spontaneous contraction, Thus, the specific muscle cell type formed was controlled by the expression of MyoD, These results provided evidence that the specific cell type formed (whether it be muscle, neuronal, or other cell types) can be controlled in vitro, Further, these results demonstrated that ES cells can provide a source of multiple differentiated cell types that can be used for transplantation. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02114. MCLEAN HOSP,NEUROREGENERAT LAB,BELMONT,MA 02178. UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA 01605. RP Dinsmore, J (reprint author), DIACRIN INC,BOSTON,MA 02129, USA. NR 56 TC 143 Z9 160 U1 0 U2 9 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0963-6897 J9 CELL TRANSPLANT JI Cell Transplant. PD MAR-APR PY 1996 VL 5 IS 2 BP 131 EP 143 DI 10.1016/0963-6897(95)02040-3 PG 13 WC Cell & Tissue Engineering; Medicine, Research & Experimental; Transplantation SC Cell Biology; Research & Experimental Medicine; Transplantation GA UB957 UT WOS:A1996UB95700003 PM 8689027 ER PT J AU Galpern, WR Frim, DM Tatter, SB Altar, CA Beal, MF Isacson, O AF Galpern, WR Frim, DM Tatter, SB Altar, CA Beal, MF Isacson, O TI Cell-mediated delivery of brain-derived neurotrophic factor enhances dopamine levels in an MPP+ rat model of substantia nigra degeneration SO CELL TRANSPLANTATION LA English DT Article; Proceedings Paper CT 2nd Annual Meeting of the American-Society-for-Neural-Transplantation CY APR 27-29, 1995 CL CLEARWATER, FL SP Amer Soc Neural Transplantat DE brain-derived neurotrophic factor; dopamine; MPP+; neuroprotection; substantia nigra ID NERVE GROWTH-FACTOR; SEPTAL CHOLINERGIC NEURONS; HUNTINGTONS-DISEASE; MESSENGER-RNAS; GENE-TRANSFER; TRANSECTION; TOXICITY; PREVENTS; DEATH; BDNF AB Brain-derived neurotrophic factor (BDNF) promotes the survival of fetal mesencephalic dopaminergic cells and protects dopaminergic neurons against the toxicity of MPP+ in vitro, Supranigral implantation of fibroblasts genetically engineered to secrete BDNF attenuates the loss of substantia nigra pars compacta (SNc) dopaminergic neurons associated with striatal infusion of MPP+ in the adult rat, Using this MPP+ rat model of nigral degeneration, we evaluated the neurochemical effects of supranigral, cell-mediated delivery of BDNF on substantia nigra (SN) dopamine (DA) content and turnover, Genetically engineered BDNF-secreting fibroblasts (similar to 12 ng BDNF/24 h) were implanted dorsal to the SN 7 days prior to striatal MPP+ administration, The present results demonstrate that BDNF-secreting fibroblasts, as compared to control fibroblasts, enhance SN DA levels ipsilateral as well as contralateral to the graft without altering DA turnover. This augmentation of DA levels suggests that local neurotrophic factor delivery by genetically engineered cells may provide a therapeutic strategy for preventing neuronal death or enhancing neuronal function in neurodegenerative diseases characterized by dopaminergic neuronal dysfunction, such as Parkinson's disease. C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,NEUROL & NEUROSURG SERV,BOSTON,MA 02114. REGENERON PHARMACEUT INC,TARRYTOWN,NY 10591. UNIV MASSACHUSETTS,MED CTR,WORCESTER,MA 01655. RP Galpern, WR (reprint author), MCLEAN HOSP,MRC 119,NEUROREGENERAT LAB,115 MILL ST,BELMONT,MA 02178, USA. FU NINDS NIH HHS [NS16367, NS29178, NS31579] NR 50 TC 53 Z9 56 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0963-6897 J9 CELL TRANSPLANT JI Cell Transplant. PD MAR-APR PY 1996 VL 5 IS 2 BP 225 EP 232 DI 10.1016/0963-6897(95)02030-6 PG 8 WC Cell & Tissue Engineering; Medicine, Research & Experimental; Transplantation SC Cell Biology; Research & Experimental Medicine; Transplantation GA UB957 UT WOS:A1996UB95700009 PM 8689033 ER PT J AU Bhol, K Yunis, J Ahmed, AR AF Bhol, K Yunis, J Ahmed, AR TI Pemphigus vulgaris in distant relatives of two families: Association with major histocompatibility complex class II genes SO CLINICAL AND EXPERIMENTAL DERMATOLOGY LA English DT Article ID JEWISH PATIENTS; ANTIGENS; FOLIACEUS; JAPANESE; HLA-DRW4 AB We describe major histocompatibility complex (MHC) class II gene haplotypes in two extended families, each of which has two members with pemphigus vulgaris (PV). One family is of Ashkenazi Jewish descent and the other family of English-Scottish descent. In one family the patients are distant relatives; in the other, both share the same mother but have different fathers. The affected relatives in the two families have never shared a common environment and live in distant states. All four PV patients, regardless of whether they were of Ashkenazi Jewish or of English-Scottish descent, had the same haplotype, namely HLA-DRB1*0402, DQA1*0301, DQB1*0302. Thus the PV patients, even though distantly related within a family, had the same MHC class II haplotype previously documented in Jewish patients. This observation further supports the concept that PV may result from an enhanced genetic susceptibility or predisposition to the disease. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. FU NEI NIH HHS [EY08379]; NIDCR NIH HHS [DE09978] NR 32 TC 7 Z9 7 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0307-6938 J9 CLIN EXP DERMATOL JI Clin. Exp. Dermatol. PD MAR PY 1996 VL 21 IS 2 BP 100 EP 103 DI 10.1046/j.1365-2230.1996.d01-197.x PG 4 WC Dermatology SC Dermatology GA UU217 UT WOS:A1996UU21700005 PM 8759194 ER PT J AU Jawahar, S Moody, C Chan, M Finberg, R Geha, R Chatila, T AF Jawahar, S Moody, C Chan, M Finberg, R Geha, R Chatila, T TI Natural killer (NK) cell deficiency associated with an epitope-deficient Fc receptor type IIIA (CD16-II) SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY LA English DT Article DE immunodeficiency; natural killer cells; Fc receptors; CD16; herpes; viruses ID GAMMA-RIII; MONOCLONAL-ANTIBODIES; ADHESION MOLECULE; EXPRESSION; INVIVO; IGG; FORMS; IDENTIFICATION; NEUTROPHILS; INFECTIONS AB Susceptibility to herpes virus infections has been described in experimental animals depleted of NK cells and in patients with defective NK cell function. We have identified a child with recurrent infections, especially with herpes simplex virus, who had a decreased number of CD56(+)CD3(-) NK cells in circulation. Her NK cells expressed an altered form of the Fc receptor for IgG type IIIA (Fc gamma RIIIA or CD16-II) which was not reactive with the anti-CD16-II MoAb B73.1. Sequence analysis revealed the patient to be homozygous for a T to A substitution at position 230 of CD16-II cDNA, predicting a Leu(66) to His(66) change in the first immunoglobulin domain of CD16-II at the B73.1 recognition site. Spontaneous NK cell activity of the patient's peripheral blood mononuclear cells (PBMC) was markedly decreased, while antibody-dependent cellular cytotoxicity (ADCC) was unaffected. These results suggest that this child suffers from a defect affecting the development and function of NK cells, resulting in NK cytopenia and clinically significant immunodeficiency. The role of the CD16-II mutant in the pathogenesis of the patient's NK cell deficiency is discussed. C1 CHILDRENS HOSP,DIV IMMUNOL,BOSTON,MA. DANA FARBER CANC INST,DIV INFECT DIS,BOSTON,MA 02115. RI Finberg, Robert/E-3323-2010 NR 31 TC 71 Z9 74 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9104 J9 CLIN EXP IMMUNOL JI Clin. Exp. Immunol. PD MAR PY 1996 VL 103 IS 3 BP 408 EP 413 PG 6 WC Immunology SC Immunology GA TZ241 UT WOS:A1996TZ24100010 PM 8608639 ER PT J AU Shimamura, A Fisher, DE AF Shimamura, A Fisher, DE TI p53 in life and death SO CLINICAL CANCER RESEARCH LA English DT Article ID WILD-TYPE P53; CELL-CYCLE ARREST; SV40-TRANSFORMED CELLS; GENE AMPLIFICATION; DNA-DAMAGE; PROTEIN; MUTATIONS; APOPTOSIS; CHECKPOINT; FORMS C1 CHILDRENS HOSP,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 56 TC 59 Z9 63 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD MAR PY 1996 VL 2 IS 3 BP 435 EP 440 PG 6 WC Oncology SC Oncology GA TY620 UT WOS:A1996TY62000001 PM 9816188 ER PT J AU Soiffer, RJ Murray, C Shapiro, C Collins, H Chartier, S Lazo, S Ritz, J AF Soiffer, RJ Murray, C Shapiro, C Collins, H Chartier, S Lazo, S Ritz, J TI Expansion and manipulation of natural killer cells in patients with metastatic cancer by low-dose continuous infusion and intermittent bolus administration of interleukin 2 SO CLINICAL CANCER RESEARCH LA English DT Article ID BONE-MARROW TRANSPLANTATION; CHRONIC MYELOGENOUS LEUKEMIA; RECOMBINANT INTERLEUKIN-2; PROLONGED INFUSION; SOLID TUMORS; EXPRESSION; RECEPTORS; TOXICITY; IMMUNOTHERAPY; ACTIVATION AB Interleukin 2 (IL-2) administered at low doses for prolonged periods can markedly expand the number of CD56(+) natural killer (NK) cells in patients with metastatic cancer. The cytotoxic capacity of NK cells obtained from patients receiving IL-2 in vivo can be dramatically augmented by additional exposure to IL-2 in vitro. These observations formed the basis of a clinical trial in which patients with metastatic cancer were treated with low-dose continuous daily infusions of IL-2 to increase the number of their NK cells in conjunction with intermittent boluses of additional IL-2 to stimulate this expanded pool of cytotoxic cells. Twenty-three patients were registered to receive IL-2 at 4.5 x 10(5) units/m(2)/day for 8 weeks by continuous i.v. infusion. After 4 weeks of ''priming'' with low-dose continuous infusion IL-2, cohorts of three to five patients received 5 weekly 2-h boluses of IL-2 at doses ranging from 2.5 x 10(5) units/m(2) to 1.0 x 10(6) units/m(2). Low-dose continuous infusion IL-2 was usually well tolerated; 2-11 bolus infusions of IL-2 were often associated with high fevers and constitutional symptoms that resolved after several hours. Low-dose continuous infusion IL-2 resulted in the progressive expansion of circulating CD56(+)CD3(-) NK cells. In contrast, each bolus infusion of IL-2 resulted in an immediate dramatic decrease in both the number of NK cells and activated T lymphocytes with recovery noted within 24 h. Bolus doses of IL-2 as low as 2.5 x 10(5) units/m(2) were capable of producing these effects. Cytolytic activity against NK-sensitive and -resistant targets correlated with the presence of circulating activated NK cells. Our results demonstrate that NK cells expanded by low-dose continuous infusions of IL-2 can be further activated in vivo by exposure to very low doses of IL-2 as a 2-h.i.v. bolus. This capacity to manipulate human NK cells in vivo through varying the dose and schedule of IL-2 administration may help in defining the therapeutic potential of these cytotoxic effecters in the treatment of both neoplastic and infectious diseases. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. RP Soiffer, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA41619]; NIAID NIH HHS [AI29530] NR 30 TC 25 Z9 25 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD MAR PY 1996 VL 2 IS 3 BP 493 EP 499 PG 7 WC Oncology SC Oncology GA TY620 UT WOS:A1996TY62000008 PM 9816195 ER PT J AU Marsh, DJ Learoyd, DL Andrew, SD Krishnan, L Pojer, R Richardson, AL Delbridge, L Eng, C Robinson, BG AF Marsh, DJ Learoyd, DL Andrew, SD Krishnan, L Pojer, R Richardson, AL Delbridge, L Eng, C Robinson, BG TI Somatic mutations in the RET proto-oncogene in sporadic medullary thyroid carcinoma SO CLINICAL ENDOCRINOLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; DNA PROBES; PROTOONCOGENE AB OBJECTIVE We have determined the frequency of specific mutations in the RET proto-oncogene in sporadic medullary thyroid carcinomas (MTCs) and correlated the presence or absence of a codon 918 mutation with the clinical characteristics of these tumours. DESIGN Thirty paraffin-embedded sporadic MTCs and two frozen MTCs were collected for analysis of specific mutations in the RET proto-oncogene in codons 609, 611, 618 and 620 (exon 10); 630 and 634 (exon 11); 768 (exon 13); 883 (exon 15) and 918 (exon 16). A novel primer was designed which introduced a restriction site for Rsal in the presence of the specific codon 918 mutation (ATG --> ACG) in these tumour samples. A 'clinical-genetic' correlation was performed comparing the presence or absence of the codon 918 mutation with the following clinical characteristics: age at diagnosis, tumour size, presence or absence of metastases, MTC related morbidity, and base line calcitonin levels at diagnosis or most recent follow-up. PATIENTS Patients were classified as having sporadic MTC if there was no family history of C-cell hyperplasia, MTC, phaeochromocytoma or parathyroid disease. Retrospective review of patient records enabled complete clinical data to be obtained in 28 of 32 patients. MEASUREMENTS Base line calcitonin levels were measured by radioimmunoassay or calcitonin enzyme linked immunoassay. Cysteine codons in exons 10 and 11, specifically codons 609, 611, 618, 620, 630 and 634, were screened for the presence of mutations by sequence analysis. Specific mutations occurring at codons 768, 883 and 918 were screened for by restriction endonuclease digestion of PCR products. RESULTS The mutation at codon 918ATG --> ACG was found in 21 of 32 (66%) MTCs and the mutation at codon 883GCT-->TTT was found in one of 32 MTCs. Where possible, the presence of 'germline-type' mutations in codons 609, 611, 618, 620, 630 and 634 were excluded. Ten MTCs did not have a mutation in codons 768, 883 or 918 of the RET proto-oncogene. The presence or absence of the somatic mutation at codon 918 did not correlate with any of the above clinical characteristics. CONCLUSION Somatic mutations in the RET protooncogene occur frequently in sporadic MTCs. C1 ROYAL N SHORE HOSP,KOLLING INST MED RES,MOLEC GENET UNIT,ST LEONARDS,NSW 2065,AUSTRALIA. ROYAL N SHORE HOSP,KOLLING INST MED RES,DEPT ENDOCRINOL,ST LEONARDS,NSW 2065,AUSTRALIA. ROYAL N SHORE HOSP,KOLLING INST MED RES,DEPT PATHOL ANAT,ST LEONARDS,NSW 2065,AUSTRALIA. ROYAL N SHORE HOSP,KOLLING INST MED RES,DEPT SURG,ST LEONARDS,NSW 2065,AUSTRALIA. UNIV SYDNEY,SYDNEY,NSW 2006,AUSTRALIA. UNIV CAMBRIDGE,ADDENBROOKES HOSP,CRC,HUMAN CANC GENET RES GRP,CAMBRIDGE,ENGLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. RI Marsh, Deborah/I-1491-2014; OI Marsh, Deborah/0000-0001-5899-4931; Eng, Charis/0000-0002-3693-5145 NR 44 TC 122 Z9 127 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0300-0664 J9 CLIN ENDOCRINOL JI Clin. Endocrinol. PD MAR PY 1996 VL 44 IS 3 BP 249 EP 257 DI 10.1046/j.1365-2265.1996.681503.x PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA TW808 UT WOS:A1996TW80800002 PM 8729519 ER PT J AU Rubin, RH Fischman, AJ AF Rubin, RH Fischman, AJ TI Radionuclide imaging of infection in the immunocompromised host SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; PNEUMOCYSTIS-CARINII PNEUMONIA; CHEMOTACTIC PEPTIDE ANALOGS; NONSPECIFIC POLYCLONAL IGG; IMMUNE-DEFICIENCY SYNDROME; GA-67 SCINTIGRAPHY; HUMAN-IMMUNOGLOBULIN; BACTERIAL-INFECTION; FOCAL INFECTION; AIDS PATIENTS AB Early diagnosis of infection in the immunocompromised patient is often difficult because of an impaired inflammatory response to microbial invasion. Radioscintigraphy has certain advantages in approaching this problem: because it is based upon either delivery of leukocytes to the site of infection or the leakiness of capillaries to radiolabeled proteins, earlier diagnosis is possible, even in patients with surgically altered anatomy; whole-body imaging allows the detection of focal sites of infection that are unsuspected clinically; and the semiquantitative nature of the information obtained allows for serial studies to assess the response to therapy. Three reagents are either currently available (gallium-67 citrate and radiolabeled leukocytes) or soon to be available (indium-111-labeled nonspecific polyclonal IgG) for this purpose. A major disadvantage of all three techniques is that a delay of 18-24 hours between injection and imaging is required. Experimental reagents such as technetium-99m-labeled chemotactic peptides appear to require <3 hours between injection and imaging. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP Rubin, RH (reprint author), HARVARD UNIV,MIT,CTR EXPTL PHARMCOL & THERAPEUT,DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02142, USA. NR 38 TC 11 Z9 11 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD MAR PY 1996 VL 22 IS 3 BP 414 EP 422 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA TY732 UT WOS:A1996TY73200002 PM 8852955 ER PT J AU Pins, MR Holden, JM Yang, JM Madoff, S Ferraro, MJ AF Pins, MR Holden, JM Yang, JM Madoff, S Ferraro, MJ TI Isolation of presumptive Streptobacillus moniliformis from abscesses associated with the female genital tract SO CLINICAL INFECTIOUS DISEASES LA English DT Article AB We report three cases in which Streptobacillus moniliformis was isolated from abscesses. Abscess material in each case contained small, pleomorphic, gram-negative to gram-variable bacilli. Anaerobic blood agar cultures yielded pinpoint colonies adjacent to small gray-white colonies. The pinpoint colonies did not gram stain, and the gray-white colonies varied from gram-variable coccobacilli to long, curly, gram-variable rods. The pinpoint colonies microscopically resembled L-forms on Dienes-stained agar preparation. Subculture to serum-supplemented thioglycolate broth demonstrated ''puff ball'' colonies. Fatty acid profiles obtained with use of gas chromatography coupled with mass spectrometry showed major peaks for C16:0, C18:2, C18:1, and C18:0 fatty acids, a profile characteristic of S. moniliformis. Results of biochemical testing of each isolate were equivocal. S. moniliformis, bacterial L-forms, and common isolates from genital tract abscesses are discussed. C1 MASSACHUSETTS GEN HOSP,MICROBIOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 17 TC 14 Z9 15 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD MAR PY 1996 VL 22 IS 3 BP 471 EP 476 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA TY732 UT WOS:A1996TY73200012 PM 8852965 ER PT J AU Stevenson, S Goldberg, VM Tomford, WV AF Stevenson, S Goldberg, VM Tomford, WV TI Papers from the International Symposium on bone and soft tissue allografts - Editorial comment SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,ORTHOPAED SERV,ORTHOPAED ONCOL UNIT,BOSTON,MA. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. RP Stevenson, S (reprint author), CASE WESTERN RESERVE UNIV,DEPT ORTHOPAED,11100 EUCLID AVE,CLEVELAND,OH 44106, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD MAR PY 1996 IS 324 BP 2 EP 4 PG 3 WC Orthopedics; Surgery SC Orthopedics; Surgery GA TX968 UT WOS:A1996TX96800001 ER PT J AU Goldring, SR Goldring, MB AF Goldring, SR Goldring, MB TI Cytokines and skeletal physiology SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article; Proceedings Paper CT International Symposium on Bone and Soft Tissue Allografts CY APR 28-30, 1995 CL WASHINGTON, DC SP Musculoskeletal Transplant Fdn ID GROWTH-FACTOR-BETA; BLOOD MONONUCLEAR-CELLS; TUMOR NECROSIS FACTORS; BONE-RESORPTION; FACTOR-ALPHA; HUMAN CHONDROCYTES; SYNOVIAL-CELLS; INTERLEUKIN-1; EXPRESSION; RECEPTOR AB Cytokines are soluble factors that play a critical role in mediating cell to cell interactions within skeletal tissues, These effects are mediated by paracrine, autocrine, and juxtacrine mechanisms, There are also examples in which the cytokines can function in an endocrine fashion, The regulatory functions of the cytokines are performed throughout life, beginning with bone growth and development and continuing in the mature organism, in which bone remodeling is regulated, The cytokines can be grouped into distinct families based on their principal biologic activity and cell target, However, the activities of the cytokines are pleiotropic, and they exhibit considerable overlap and redundancy in their actions, The molecular cloning of the cytokines and their receptors and elucidation of their common structural features have aided in the understanding of the molecular basis for the redundancy and pleiotropy of cytokine effects, Examination of most physiologic processes in which cytokines play an important regulatory role reveals that cytokines rarely exert their biologic activities in isolation, Instead, these soluble factors usually are produced locally in concert with many other cytokines, The interaction of these structurally and functionally distinct factors in a highly ordered temporal and spatial sequence creates a cytokine network that ultimately determines a given tissue's response, Continued investigation into the molecular and biologic mechanisms by which cytokines regulate bone cell function will provide additional insights into normal bone physiology and permit more effective and specific use of these factors in the treatment of skeletal disorders. C1 NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. NEW ENGLAND BONE & JOINT INST,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,MED SERV,ARTHRITIS UNIT,BOSTON,MA. NR 66 TC 30 Z9 31 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD MAR PY 1996 IS 324 BP 13 EP 23 PG 11 WC Orthopedics; Surgery SC Orthopedics; Surgery GA TX968 UT WOS:A1996TX96800003 PM 8595748 ER PT J AU Mankin, HJ Gebhardt, MC Jennings, LC Springfield, DS Tomford, WW AF Mankin, HJ Gebhardt, MC Jennings, LC Springfield, DS Tomford, WW TI Long-term results of allograft replacement in the management of bone tumors SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article; Proceedings Paper CT International Symposium on Bone and Soft Tissue Allografts CY APR 28-30, 1995 CL WASHINGTON, DC SP Musculoskeletal Transplant Fdn ID OSTEO-SARCOMA; ADJUVANT CHEMOTHERAPY; MASSIVE ALLOGRAFTS; TRANSPLANTATION; RECONSTRUCTION; RESECTIONS; SURGERY; SYSTEM; TIBIA; TRIAL AB Over the past 24 years, the authors have implanted >870 massive frozen cadaveric allografts mostly for the treatment of defects created by the resection of a bone turner, Most of the grafts were obtained from the authors' institutional bone bank, The results show that only stage and type of graft affected outcome predictably, Specifically, grafts for a Stage 2 or Stage 3 tumor had a poorer outcome than those for Stages 0 and 1, The results for allograft arthrodeses were considerably poorer than osteoarticular, intercalary, and allograft plus prosthesis, The other major factors in results were complications-recurrence, infection, fracture, and nonunion-with the former 2 having a profound negative effect on outcome, After the first year of susceptibility to infection (10%) and the third year of increased risk of fracture (19%), the grafts become stable, and approximately 75% are retained by patients and are considered to be successful for >20 years after implantation, Osteoarthritis becomes a problem at approximately 6 years for osteoarticular grafts, and so far, 16% of the patients with distal femoral, proximal tibial, or proximal femoral grafts have required total joint replacements, Although the current results are adequate, they are imperfect, and research should be directed at improving the results. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. RP Mankin, HJ (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED SERV,ORTHOPAED ONCOL UNIT,GRAY 606,BOSTON,MA 02114, USA. NR 62 TC 337 Z9 371 U1 2 U2 11 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD MAR PY 1996 IS 324 BP 86 EP 97 PG 12 WC Orthopedics; Surgery SC Orthopedics; Surgery GA TX968 UT WOS:A1996TX96800011 PM 8595781 ER PT J AU Scully, SP Temple, HT OKeefe, RJ Mankin, HJ Gebhardt, M AF Scully, SP Temple, HT OKeefe, RJ Mankin, HJ Gebhardt, M TI The surgical treatment of patients with osteosarcoma who sustain a pathologic fracture SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID OSTEOGENIC-SARCOMA; EXPERIENCE AB The presence of pathologic fracture in osteosarcoma raises concerns of tumor dissemination by the fracture hematoma and has been considered a contraindication to limb salvage surgery, Because this is a theoretical concern, there are little clinical data available in the literature on which to base treatment of these patients, Eighteen patients with osteosarcoma who sustained a pathologic fracture and had a minimum of 24 months of followup were reviewed retrospectively. Surgical treatment included nonoperative therapy, amputation, and limb salvage groups, Patients who refused surgical intervention (2) had a uniformly poor outcome, Patients who underwent amputation (6) had no local recurrences and 33% developed metastases. Patients who underwent limb salvage (10) experienced 3 local recurrences and 6 distant recurrences, Although the distant recurrence rate for patients undergoing amputation was no different from the rate for those undergoing limb salvage, the difference in local tumor control approached statistical significance, All patients who developed local recurrence died, Surgical treatment needs to be individualized and based on factors such as fracture displacement, stability, radiographic and histologic response to chemotherapy, and the perceived ability to resect the fracture hematoma completely. C1 UNIV ROCHESTER,ROCHESTER,NY. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. MASSACHUSETTS GEN HOSP,ORTHOPAED ONCOL UNIT,BOSTON,MA 02114. RP Scully, SP (reprint author), DUKE UNIV,MED CTR,BOX 3312,DURHAM,NC 27710, USA. NR 10 TC 40 Z9 43 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD MAR PY 1996 IS 324 BP 227 EP 232 PG 6 WC Orthopedics; Surgery SC Orthopedics; Surgery GA TX968 UT WOS:A1996TX96800028 PM 8595761 ER PT J AU Pagano, M Murphy, JM Pedersen, M Mosbacher, D CristWhitzel, J Jordan, P Rodas, C Jellinek, MS AF Pagano, M Murphy, JM Pedersen, M Mosbacher, D CristWhitzel, J Jordan, P Rodas, C Jellinek, MS TI Screening for psychosocial problems in 4-5-year-olds during routine EPSDT examinations: Validity and reliability in a Mexican-American sample SO CLINICAL PEDIATRICS LA English DT Article ID PEDIATRIC PRIMARY CARE; MENTAL-HEALTH SERVICES; SYMPTOM CHECKLIST; RISK-FACTORS; CHILDREN; PSYCHOPATHOLOGY; DYSFUNCTION; PREVALENCE; PHYSICIANS; VALIDATION AB The effectiveness of the Pediatric Symptom Checklist (PSC) as a psychosocial screening measure to meet Federal Medicaid/Early and Periodic Screening, Diagnosis, and Treatment (EPSDT) requirements was examined in 117 low-income preschool (aged 4-5 years old) Hispanic children during well-child examinations in three clinics over an 8-month period, The PSC identified 7% of the sample as at risk for psychosocial problems, The PSC was significantly associated with parental ratings of the children's problems in functioning, with pediatric clinicians' decisions to make mental health referrals, with degrees of associations similar to those found between PSC scores, and with the same measures with school-aged children in the same clinics, Cronbach's alpha was high (r=.87) and virtually identical in English, Spanish, oral, and written formats, Although it identified a slightly lower rate of psychosocial problems in 4-5-year-olds than it had in school-aged children, the PSC appeared to provide an effective method of screening for psychosocial problems during EPSDT examinations. C1 MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,BOSTON,MA 02114. FU NIAAA NIH HHS [L30 AA014994, L30 AA014994-03] NR 56 TC 22 Z9 22 U1 2 U2 2 PU WESTMINSTER PUBL INC PI GLEN HEAD PA 708 GLEN COVE AVE, GLEN HEAD, NY 11545 SN 0009-9228 J9 CLIN PEDIATR JI Clin. Pediatr. PD MAR PY 1996 VL 35 IS 3 BP 139 EP 146 DI 10.1177/000992289603500305 PG 8 WC Pediatrics SC Pediatrics GA TZ388 UT WOS:A1996TZ38800005 PM 8904487 ER PT J AU Serratosa, JM DelgadoEscueta, AV AF Serratosa, JM DelgadoEscueta, AV TI Mapping human epilepsy genes - Implications for the treatment of epilepsy SO CNS DRUGS LA English DT Article ID FAMILIAL NEONATAL CONVULSIONS; MYOCLONIC EPILEPSY; ASSIGNMENT; DISEASE AB Recent and ongoing advances in mapping and isolating human epilepsy genes will: (i) modify the classification of the epilepsies; (ii) base antiepileptic drug development on defined epilepsy mutations; and (iii) spur the development of somatic cell and/or germ line therapy for the fatal progressive myoclonus epilepsies and, eventually, the chronic generalised and partial epilepsies. In the next century, advances in these 3 areas will dramatically change the diagnostic, therapeutic and prognostic approach to patients with epilepsy, and will probably eliminate some genetic epilepsies within 2 or 3 generations. C1 W LOS ANGELES DVA MED CTR,COMPREHENS EPILEPSY PROGRAM 127B,NEUROL SERV,LOS ANGELES,CA 90073. W LOS ANGELES DVA MED CTR,COMPREHENS EPILEPSY PROGRAM 127B,RES SERV,LOS ANGELES,CA 90073. NR 19 TC 4 Z9 4 U1 0 U2 0 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1172-7047 J9 CNS DRUGS JI CNS Drugs PD MAR PY 1996 VL 5 IS 3 BP 155 EP 159 PG 5 WC Clinical Neurology; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA UA225 UT WOS:A1996UA22500001 ER PT J AU Baldassano, CF Truman, CJ Nierenberg, A Ghaemi, SN Sachs, GS AF Baldassano, CF Truman, CJ Nierenberg, A Ghaemi, SN Sachs, GS TI Akathisia: A review and case report following paroxetine treatment SO COMPREHENSIVE PSYCHIATRY LA English DT Article ID NEUROLEPTIC-INDUCED AKATHISIA; TARDIVE-DYSKINESIA; SUICIDE ATTEMPTS; PROPRANOLOL; FLUOXETINE; SERTRALINE; POPULATION; DISORDERS; DRUGS AB Although akathisia is most commonly associated with neuroleptic medication, few cases of paroxetine-induced akathisia have been reported. A review of the authors' charts (C.F.B., A.N., S.N.G., and G.S.S.) was conducted to determine an estimated incidence for paroxetine-induced akathisia. Three cases of akathisia were reported in 67 patients treated with paroxetine. A case of akathisia secondary to paroxetine in an 18-year-old female is presented. Given the potential untoward effects of this syndrome, early diagnosis is essential. Clinical presentations and differential diagnoses are discussed. Copyright (C) 1996 by W.B. Saunders Company C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,CAMBRIDGE,MA 02138. RP Baldassano, CF (reprint author), MASSACHUSETTS GEN HOSP,WANG AMBULATORY CARE CTR,PSYCHOPHARMACOL CLIN,ROOM 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 40 TC 30 Z9 30 U1 0 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0010-440X J9 COMPR PSYCHIAT JI Compr. Psychiat. PD MAR-APR PY 1996 VL 37 IS 2 BP 122 EP 124 DI 10.1016/S0010-440X(96)90572-6 PG 3 WC Psychiatry SC Psychiatry GA TZ144 UT WOS:A1996TZ14400007 PM 8654061 ER PT J AU Ahern, DK AF Ahern, DK TI Psychophysiological disorders: Research and clinical applications - Gatchel,RJ, Blanchard,EB SO CONTEMPORARY PSYCHOLOGY LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP Ahern, DK (reprint author), MASSACHUSETTS GEN HOSP,BEHAV MED UNIT,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD MAR PY 1996 VL 41 IS 3 BP 240 EP 241 PG 2 WC Psychology, Multidisciplinary SC Psychology GA TZ146 UT WOS:A1996TZ14600018 ER PT J AU Faber, R AF Faber, R TI Electroconvulsive therapy in parkinson's disease and other movement disorders. SO CONVULSIVE THERAPY LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 2 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0749-8055 J9 CONVULSIVE THER JI Convulsive Therapy PD MAR PY 1996 VL 12 IS 1 BP 65 EP 65 PG 1 WC Psychiatry SC Psychiatry GA UP329 UT WOS:A1996UP32900017 ER PT J AU Haas, J Park, EC Seed, B AF Haas, J Park, EC Seed, B TI Codon usage limitation in the expression of HIV-1 envelope glycoprotein SO CURRENT BIOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; REV-RESPONSE ELEMENT; STRUCTURAL GENE-EXPRESSION; GREEN-FLUORESCENT PROTEIN; VIRAL MESSENGER-RNA; LINEAR DUPLEX DNA; ESCHERICHIA-COLI; TRANS-ACTIVATOR; RESPECTIVE CODONS; TARGET SEQUENCE AB Background: The expression of both the env and gag gene products of human immunodeficiency virus type 1 (HIV-I) is known to be limited by cis elements in the viral RNA that impede egress from the nucleus and reduce the efficiency of translation, Identifying these elements has proven difficult, as they appear to be disseminated throughout the viral genome. Results: Here, we report that selective codon usage appears to account for a substantial fraction of the inefficiency of viral protein synthesis, independent of any effect on improved nuclear export, The codon usage effect is not specific to transcripts of HIV-1 origin. Re-engineering the coding sequence of a model protein (Thy-1) with the most prevalent HIV-1 codons significantly impairs Thy-1 expression, whereas altering the coding sequence of the jellyfish green fluorescent protein gene to conform to the favored codons of highly expressed human proteins results in a substantial increase in expression efficiency, Conclusions: Codon-usage effects are a major impediment to the efficient expression of HIV-I genes, Although mammalian genes do not show as profound a bias as do Escherichia coli genes, other proteins that are poorly expressed in mammalian cells can benefit from codon re-engineering. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MELVIN & BARBARA NESSEL GENE THERAPY CTR,BOSTON,MA 02114. FU NHLBI NIH HHS [HL53694] NR 64 TC 375 Z9 393 U1 1 U2 27 PU CURRENT BIOLOGY LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD MAR 1 PY 1996 VL 6 IS 3 BP 315 EP 324 DI 10.1016/S0960-9822(02)00482-7 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UC440 UT WOS:A1996UC44000026 PM 8805248 ER PT J AU Chiu, WL Niwa, Y Zeng, W Hirano, T Kobayashi, H Sheen, J AF Chiu, WL Niwa, Y Zeng, W Hirano, T Kobayashi, H Sheen, J TI Engineered GFP as a vital reporter in plants SO CURRENT BIOLOGY LA English DT Article ID ARABIDOPSIS-THALIANA; PROTEIN; MAIZE; EXPRESSION; GENE; PROMOTERS; TRANSIENT AB Background: The green-fluorescent protein (GFP) of the jellyfish Aequorea victoria has recently been used as a universal reporter in a broad range of heterologous living cells and organisms. Although successful in some plant transient expression assays based on strong promoters or high copy number viral vectors, further improvement of expression efficiency and fluorescent intensity are required for GFP to be useful as a marker in intact plants. Here, we report that an extensively modified GFP is a versatile and sensitive reporter in a variety of living plant cells and in transgenic plants. Results: We show that a re-engineered GFP gene sequence, with the favored codons of highly expressed human proteins, gives 20-fold higher GFP expression in maize leaf cells than the original jellyfish GFP sequence. When combined with a mutation in the chromophore, the replacement of the serine at position 65 with a threonine, the new GFP sequence gives more than 100-fold brighter fluorescent signals upon excitation with 490 nm (blue) light, and swifter chromophore formation, We also show that this modified GFP has a broad use in various transient expression systems, and allows the easy detection of weak promoter activity, visualization of protein targeting into the nucleus and various plastids, and analysis of signal transduction pathways in living single cells and in transgenic plants. Conclusions: The modified GFP is a simple and economical new tool for the direct visualization of promoter activities with a broad range of strength and cell specificity. It can be used to measure dynamic responses of signal transduction pathways, transfection efficiency, and subcellular localization of chimeric proteins, and should be suitable for many other applications in genetically modified living cells and tissues of higher plants. The data also suggest that the codon usage effect might be universal, allowing the design of recombinant proteins with high expression efficiency in evolutionarily distant species such as humans and maize. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT MOLEC BIOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT GENET, BOSTON, MA 02114 USA. UNIV SHIZUOKA, SCH FOOD & NUTR SCI, SHIZUOKA 422, JAPAN. RI Kobayashi, Hirokazu/E-7903-2010 OI Kobayashi, Hirokazu/0000-0002-8040-0826 NR 39 TC 1006 Z9 1041 U1 15 U2 134 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0960-9822 J9 CURR BIOL JI Curr. Biol. PD MAR 1 PY 1996 VL 6 IS 3 BP 325 EP 330 DI 10.1016/S0960-9822(02)00483-9 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA UC440 UT WOS:A1996UC44000027 PM 8805250 ER PT J AU Donaghue, VM Sarnow, MR Giurini, JM Chrzan, JS Habershaw, GM Veves, A AF Donaghue, VM Sarnow, MR Giurini, JM Chrzan, JS Habershaw, GM Veves, A TI Longitudinal in-shoe foot pressure relief achieved by specially designed footwear in high risk diabetic patients SO DIABETES RESEARCH AND CLINICAL PRACTICE LA English DT Article DE footwear; foot pressure; at risk foot ID ULCERATION; REDUCTION AB Specially designed Thor-Lo footwear has been shown to reduce the in-shoe fool pressures in diabetic patients at risk of foot ulceration when compared to their own footwear. Fifty al high risk patients 32 (64%) males, 17 (34%) type 1 diabetes) have been provided with this foot wear and have been followed up for 6 months. Mean age was 57.6 (range, 34-78) years, duration of diabetes 22.4 (range, 4-50) years, Neuropathy Symptom Score 3.36 +/- 2.96 (mean +/- S.D.), Neuropathy Disability Score 16.8 +/- 6.83, VPT 43.4 +/- 11.8 Volts while 43 (86%) could not feel a 5.07 or smaller Semmes-Weinstein monofilament. Forty-two (84%) patients were re-examined at an interim visit 3 months after baseline, while 37 (74%) completed the study. In-shoe peak forces and pressures were measured using the F-Scan system. No difference was found among the peak force among baseline (95.5 +/- 26 kg), interim (96.5 +/- 33) and final visit (97.7 +/- 25.2, P = NS). There was no difference in peak pressures at the baseline (3.98 +/- 1.42 kg . cm(-2)), second visit (4.13 +/- 2.30) and the final visit (4.25 +/- 1.51). Nine (18%) patients developed foot problems and one died during the study. We conclude that no changes in fool pressures were found over a period of 6 months of continuous usage of the specially designed footwear in a group of diabetic patients at risk of foot ulceration. Further prospective studies are required to evaluate the impact of specially designed foot ear in reducing the rate of foot ulceration. C1 HARVARD UNIV,SCH MED,DEACONESS JOSLIN FOOT CTR,DEPT MED,BOSTON,MA 02215. DEACONESS JOSLIN FOOT CTR,DEPT SURG,DIV PODIATRY,BOSTON,MA 02115. NR 22 TC 16 Z9 17 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0168-8227 J9 DIABETES RES CLIN PR JI Diabetes Res. Clin. Pract. PD MAR PY 1996 VL 31 IS 1-3 BP 109 EP 114 DI 10.1016/0168-8227(96)01211-9 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA UX402 UT WOS:A1996UX40200014 PM 8792109 ER PT J AU Veves, A Donaghue, VM Sarnow, MR Giurini, JM Campbell, DR LoGerfo, FW AF Veves, A Donaghue, VM Sarnow, MR Giurini, JM Campbell, DR LoGerfo, FW TI The impact of reversal of hypoxia by revascularization on the peripheral nerve function of diabetic patients SO DIABETOLOGIA LA English DT Article DE hypoxia; revascularization; peripheral neuropathy ID SURAL NERVE; CAPILLARY ABNORMALITIES; NEUROPATHY; POLYNEUROPATHY; CRITERIA; FOOT AB Hypoxia is considered to be one of the main aetiopathogenic factors of diabetic neuropathy. We have examined the effects of the reversal of hypoxia, achieved by revascularization, on peripheral nerve function in diabetic patients with or without clinical neuropathy. Fifty-six patients [mean age 62 (range 30-74) years, 44 (79%) males, 15 (27%) with insulin-dependent diabetes of 20 years (range 1-57) duration, and creatinine level 92.8 +/- 30.9 mu mol/l (mean +/- SD)] were tested pre-operatively while 30 (54%) were reexamined at least 6 weeks post-operatively. At baseline the leg scheduled for operation showed worse measurements compared to the control leg when tested for Semmes-Weinstein monofilaments, peroneal motor conduction velocity (PMCV) (33.7 +/- 7.18 vs 35.7 +/- 6.09 m . s(-1), p < 0.05) and transcutaneous oxygen tension (37.4 +/- 24.6 vs 52.0 +/- 21.5 mm Hg, p < 0.0001) while no differences were found in the vibration perception threshold and leg temperature. When baseline and post-operative measurements were later compared in the operated leg, no differences were noticed in the vibration perception threshold, PMCV and Semmes-Weinstein monofilaments but the transcutaneous oxygen tension increased significantly (32.7 +/- 27.1 vs 64.6 +/- 14.5 mm Hg, p < 0.001). No differences were noticed in any of the above parameters in the contralateral leg. No correlations were found between changes in transcutaneous oxygen tension and PMCV values measured at baseline and at the follow-up visit in either leg. Similar results were found when patients were stratified according to severity of neuropathy, ischaemia and the level of the bypass. We conclude that although there is greater impairment of nerve function in the more ischaemic leg, reversal of hypoxia does not result in any significant improvement of the nerve function measurements. C1 HARVARD UNIV,SCH MED,DEACONESS JOSLIN FOOT CTR,DEPT SURG,DIV PODIATRY,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEACONESS JOSLIN FOOT CTR,DEPT SURG,DIV VASC SURG,BOSTON,MA 02215. RP Veves, A (reprint author), HARVARD UNIV,SCH MED,DEACONESS JOSLIN FOOT CTR,DEPT MED,185 PILGRIM RD,BOSTON,MA 02215, USA. NR 26 TC 18 Z9 19 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD MAR PY 1996 VL 39 IS 3 BP 344 EP 348 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA TX951 UT WOS:A1996TX95100014 PM 8721781 ER PT J AU Larson, C Cavuto, NJ Flockhart, DA Weinberg, RB AF Larson, C Cavuto, NJ Flockhart, DA Weinberg, RB TI Bioavailability and efficacy of omeprazole given orally and by nasogastric tube SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE omeprazole; gastric acid secretion; nasogastric tube; pharmacokinetics; pentagastrin; cytochrome P-450; bioavailability ID ACID-SECRETION; S-MEPHENYTOIN; GASTRIC-ACID; HYDROXYLATION; POLYMORPHISM; DEBRISOQUIN; POPULATIONS; INHIBITOR; SINGLE AB We compared the bioavailability and the efficacy of omeprazole provided either as encapsulated enteric-coated granules or as enteric-coated granules delivered via a nasogastric tube in 10 healthy subjects. Omeprazole reduced mean pentagastrin-stimulated peak gastric acid secretion by 85.5% +/- 23.7% when delivered orally and by 79.6% +/- 32.1% when delivered by nasogastric tube; the mean plasma omeprazole concentration area under the curve (AUG) was 2.02 +/- 0.79 after oral delivery and 1.74 +/- 1.89 after nasogastric tube delivery. There was no significant difference in these parameters between the two routes of administration, and there was excellent intrasubject correlation between oral and nasogastric percent acid suppression and AUC. There was a close correlation between AUC and percent acid suppression at AUC values below 0.6, and complete acid suppression at AUC values above 0.6, regardless of the delivery route. We conclude that omeprazole delivered as enteric-coated granules via nasogastric tube provides equal bioavailability and gastric acid suppression as omeprazole given orally in its proprietary formulation. C1 WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT INTERNAL MED,GASTROENTEROL SECT,WINSTON SALEM,NC 27157. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,DIV GASTROENTEROL,BOSTON,MA 02114. GEORGETOWN UNIV,MED CTR,DEPT MED,DIV CLIN PHARMACOL,WASHINGTON,DC 20007. GEORGETOWN UNIV,MED CTR,DEPT PHARMACOL,DIV CLIN PHARMACOL,WASHINGTON,DC 20007. FU NCRR NIH HHS [M01-RR07122] NR 23 TC 34 Z9 35 U1 0 U2 3 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD MAR PY 1996 VL 41 IS 3 BP 475 EP 479 DI 10.1007/BF02282321 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UB267 UT WOS:A1996UB26700005 PM 8617118 ER PT J AU Mao, CA Siegler, EL Abrutyn, E AF Mao, CA Siegler, EL Abrutyn, E TI Epidemiology - Antimicrobial resistance patterns in long term geriatric care - Implications for drug therapy SO DRUGS & AGING LA English DT Article ID NURSING-HOME PATIENTS; STAPHYLOCOCCUS-AUREUS NASAL; SPECTRUM BETA-LACTAMASES; ENTEROCOCCUS-FAECIUM; ESCHERICHIA-COLI; STREPTOCOCCUS-FAECALIS; ANTIBIOTIC-RESISTANCE; NOSOCOMIAL INFECTION; ACTIVE EFFLUX; COLONIZATION AB There is a high prevalence of bacterial infections in long term care facilities (4.4 to 16.2%). This, together with the fact that antimicrobial resistance is a big concern in current medical practice, makes infection control so important in nursing home care. This article covers the mechanisms of antibacterial resistance and focuses on 4 major antibacterial-resistant bacteria. Vancomycin is the treatment of choice for methicillin-resistant Staphylococcus aureus (MRSA). Colonisation with MRSA is not uncommon in nursing homes and eradication is probably not necessary. Any clinically important enterococcal infection should be tested for high-level resistance. An infectious disease consultation should be sought for vancomycin-resistant enterococcal infections. Gram-negative bacilli have developed multiresistance. Susceptibility testing can identify the most appropriate therapy. Multiresistance should also be considered when treating Streptococcus pneumoniae. Overall, handwashing is highly recommended. Barrier precautions, minimising hospitalisations and avoiding unnecessary personnel rotation can reduce the chance of resistance spread. C1 HOSP UNIV PENN,DIV GERIATR MED,PHILADELPHIA,PA 19104. NYU,BROOKLYN HOSP CTR,SCH MED,GERIATR SECT,BROOKLYN,NY. DEPT VET AFFAIRS MED CTR,MED COLL PENN,DEPT MED,PHILADELPHIA,PA 19104. NR 66 TC 4 Z9 6 U1 1 U2 1 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1170-229X J9 DRUG AGING JI Drugs Aging PD MAR PY 1996 VL 8 IS 3 BP 162 EP 170 DI 10.2165/00002512-199608030-00002 PG 9 WC Geriatrics & Gerontology; Pharmacology & Pharmacy SC Geriatrics & Gerontology; Pharmacology & Pharmacy GA UA851 UT WOS:A1996UA85100002 PM 8720742 ER PT J AU Rosenbek, JC Robbins, JA Roecker, EB Coyle, JL Wood, JL AF Rosenbek, JC Robbins, JA Roecker, EB Coyle, JL Wood, JL TI A penetration aspiration scale SO DYSPHAGIA LA English DT Article DE dysphagia; aspiration; penetration; scaling; deglutition; deglutition disorders AB The development and use of an 8-point, equal-appearing interval scale to describe penetration and aspiration events are described. Scores are determined primarily by the depth to which material passes in the airway and by whether or not material entering the airway is expelled. Intra- and interjudge reliability have been established. Clinical and scientific uses of the scale are discussed. C1 UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,SCH MED,DEPT MED,MADISON,WI 53705. UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,SCH MED,DEPT BIOSTAT,MADISON,WI 53705. RP Rosenbek, JC (reprint author), UNIV WISCONSIN,WILLIAM S MIDDLETON MEM VET HOSP,SCH MED,DEPT NEUROL,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 11 TC 559 Z9 600 U1 1 U2 26 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0179-051X J9 DYSPHAGIA JI Dysphagia PD SPR PY 1996 VL 11 IS 2 BP 93 EP 98 DI 10.1007/BF00417897 PG 6 WC Otorhinolaryngology SC Otorhinolaryngology GA UA576 UT WOS:A1996UA57600004 PM 8721066 ER PT J AU Weber, AL Sabates, NR AF Weber, AL Sabates, NR TI Survey of CT and MR imaging of the orbit SO EUROPEAN JOURNAL OF RADIOLOGY LA English DT Article DE orbit, radiography; magnetic resonance (MR) imaging, orbit; computed tomography (CT), orbit ID COMPUTED-TOMOGRAPHY; SINUSES; TUMORS RP Weber, AL (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT RADIOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 27 TC 5 Z9 7 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0720-048X J9 EUR J RADIOL JI Eur. J. Radiol. PD MAR PY 1996 VL 22 IS 1 BP 42 EP 52 DI 10.1016/0720-048X(96)00737-1 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA UK042 UT WOS:A1996UK04200008 PM 8860703 ER PT J AU Sanchez, R Weber, AL Alexander, A Sweriduk, S Vici, G AF Sanchez, R Weber, AL Alexander, A Sweriduk, S Vici, G TI Paraorbital lesions SO EUROPEAN JOURNAL OF RADIOLOGY LA English DT Review DE skull, radiography; orbit, abnormalities; paranasal, abnormalities; paranasal, radiography ID PARA-NASAL SINUSES; COMPUTED-TOMOGRAPHY; PARANASAL SINUSES; MUCOCELES; CT; TUMORS; CAVITY; NOSE C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT RADIOL,BOSTON,MA 02114. NR 29 TC 1 Z9 4 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0720-048X J9 EUR J RADIOL JI Eur. J. Radiol. PD MAR PY 1996 VL 22 IS 1 BP 53 EP 67 DI 10.1016/0720-048X(96)00739-5 PG 15 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA UK042 UT WOS:A1996UK04200009 PM 8860704 ER PT J AU Weber, AL AF Weber, AL TI Imaging of the skull base SO EUROPEAN JOURNAL OF RADIOLOGY LA English DT Article DE skull, radiography; skull, abnormalities; skull, MR; skull, CT; magnetic resonance (MR) imaging, skull; computed tomography (CT), skull ID PERINEURAL TUMOR EXTENSION; COMPUTED-TOMOGRAPHY; INTRACRANIAL EXTENSION; FIBROUS DYSPLASIA; TRIGEMINAL NERVE; TEMPORAL BONE; MR; CT; CEPHALOCELES; FEATURES RP Weber, AL (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT RADIOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 68 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0720-048X J9 EUR J RADIOL JI Eur. J. Radiol. PD MAR PY 1996 VL 22 IS 1 BP 68 EP 81 DI 10.1016/0720-048X(96)00738-3 PG 14 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA UK042 UT WOS:A1996UK04200010 PM 8860705 ER PT J AU Phelps, DS Umstead, TM Rose, RM Fishman, JA AF Phelps, DS Umstead, TM Rose, RM Fishman, JA TI Surfactant protein-A levels increase during Pneumocystis carinii pneumonia in the rat SO EUROPEAN RESPIRATORY JOURNAL LA English DT Article DE corticosteroid; lung; opportunistic infection; phagocytosis; surfactant protein-A ID ALVEOLAR MACROPHAGES; PULMONARY SURFACTANT; PHAGOCYTOSIS; INFECTION AB In bronchoalveolar lavage (BAL) of human immunodeficiency virus (HIV)-infected patients with Pneumocystis carinii pneumonia and in lungs of glucocorticoid-immunosuppressed rats infected with P. carinii, surfactant phospholipid levels are reduced, However, levels of the surfactant-associated protein-A (SP-A) in BAL are 4-5 times higher than normal in patients with P. carinii pneumonia, In this study, we examined the effects of glucocorticoid immunosuppression and P. carinii infection on SP-A messenger ribonucleic acid (mRNA) and protein levels in rat lungs. Rats were immunosuppressed by adding dexamethasone to their drinking water and were infected with P. carinii by intratracheal instillation of the organism, SPA was measured by enzyme-linked immunosorbent assay (ELISA) and SP-A mRNA by hybridization of Northern blots with an SP-A complementary deoxyribonucleic acid (cDNA) probe. There was a severalfold increase in SP-A protein and mRNA levels in uninfected glucocorticoid-treated rats. However, contrary to what has been reported with the surfactant-associated lipids, SP-A mRNA and protein levels in P. carinii-infected animals were significantly higher than those found in the uninfected, immunosuppressed animals. Our results demonstrate that SP-A increases, probably as a result of elevated mRNA levels, in immunosuppressed rats with P. carinii infection and are consistent with our findings in HIV-positive patients with P. carinii pneumonia. C1 CYTEL CORP,LA JOLLA,CA. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. RP Phelps, DS (reprint author), PENN STATE UNIV,COLL MED,DEPT PEDIAT,POB 850,HERSHEY,PA 17033, USA. FU NHLBI NIH HHS [HL 43510, HL 48006] NR 29 TC 29 Z9 29 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0903-1936 J9 EUR RESPIR J JI Eur. Resp. J. PD MAR PY 1996 VL 9 IS 3 BP 565 EP 570 DI 10.1183/09031936.96.09030565 PG 6 WC Respiratory System SC Respiratory System GA UE474 UT WOS:A1996UE47400029 PM 8730021 ER PT J AU Seifer, DB LambertMesserlian, GM Canick, JA Frishman, GN Schneyer, AL AF Seifer, DB LambertMesserlian, GM Canick, JA Frishman, GN Schneyer, AL TI Serum inhibin levels are lower in ectopic than intrauterine spontaneously conceived pregnancies SO FERTILITY AND STERILITY LA English DT Article DE ectopic; serum total inhibin; serum dimeric inhibin ID HUMAN CHORIONIC-GONADOTROPIN; IMMUNOACTIVE INHIBIN; PROGESTERONE AB Objective: To determine if serum inhibin concentrations are lower in ectopic (EP) versus intrauterine pregnancies (IUPs) that are conceived spontaneously. Design: Case-control study. Setting: Academic clinical practice. Patients: Serum samples were obtained from 19 women who had EP confirmed at surgery and by pathology. For comparison, serum samples were collected from 24 women of similar chronological and gestational age with sonographic evidence of an IUP. Main Outcome Measure: Serum dimeric inhibin-A, total inhibin, P, and hCG. Results: Serum total and dimeric inhibin concentrations in women with EP were <60% of the concentrations for women with single IUPs. Total inhibin, but not dimeric inhibin-A, was elevated in maternal serum before week 8 of gestation relative to normal menstrual cycle levels. Conclusions: Serum inhibin concentrations are lower in EP as compared with IUPs that are spontaneously conceived and the relative amounts of dimeric inhibin-A, B, and alpha inhibin subunit in maternal serum may change throughout gestation. C1 BROWN UNIV,SCH MED,PROVIDENCE,RI 02912. MASSACHUSETTS GEN HOSP,NATL CTR INFERTIL RES,REPROD ENDOCRINE UNIT,BOSTON,MA 02114. OI Seifer, David/0000-0003-3950-9341; Messerlian, Geralyn/0000-0002-9440-3411 FU NIA NIH HHS [AG00566]; NICHD NIH HHS [HD29164] NR 7 TC 17 Z9 18 U1 0 U2 0 PU AMER SOC REPRODUCTIVE MEDICINE PI BIRMINGHAM PA 1209 MONTGOMERY HIGHWAY, BIRMINGHAM, AL 35216-2809 SN 0015-0282 J9 FERTIL STERIL JI Fertil. Steril. PD MAR PY 1996 VL 65 IS 3 BP 667 EP 669 PG 3 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA TW842 UT WOS:A1996TW84200038 PM 8774307 ER PT J AU Singaram, C SenGupta, A AF Singaram, C SenGupta, A TI Histopathology of the enteric neuropathies - From silver staining to immunohistochemistry SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA LA English DT Article ID VASOACTIVE INTESTINAL POLYPEPTIDE; NITRIC-OXIDE SYNTHASE; GENE-RELATED PEPTIDE; CELL LUNG-CARCINOMA; PIG SMALL-INTESTINE; HIRSCHSPRUNGS-DISEASE; GASTROINTESTINAL-TRACT; ELECTRON-MICROSCOPY; VISCERAL NEUROPATHY; INTERSTITIAL-CELLS AB The gut is abundantly supplied with neurons, extrinsic and intrinsic nerve fibers. Knowledge regarding the structure of the enteric nervous system derives principally from the classic silver-staining methods. Because silver stains do not provide information on the molecular constituents of neurons, these data only facilitate classification and may have diagnostic significance. Studies using histochemistry and immunohistochemistry are now completing the morphologic picture and laying the groundwork for the formulation of therapeutic strategies based upon demonstrable chemical defects in enteric disease. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI USA. BOSTON UNIV, SCH MED, BETH ISRAEL HOSP, BOSTON, MA USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. RP Singaram, C (reprint author), UNIV WISCONSIN, DIV GASTROENTEROL, H6-516 CSC, 600 HIGHLAND AVE, MADISON, WI 53792 USA. NR 87 TC 3 Z9 3 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0889-8553 J9 GASTROENTEROL CLIN N JI Gastroenterol. Clin. North Am. PD MAR PY 1996 VL 25 IS 1 BP 183 EP + DI 10.1016/S0889-8553(05)70371-X PG 0 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA UB045 UT WOS:A1996UB04500011 PM 8682572 ER PT J AU Goldberg, RJ Daly, J Backstrom, D AF Goldberg, RJ Daly, J Backstrom, D TI Psychiatric complications and comorbidities in medical inpatients - The inadequacy of attestation at discharge SO GENERAL HOSPITAL PSYCHIATRY LA English DT Article ID LIAISON PSYCHIATRY; HOSPITAL STAY; CONSULTATION; DEPRESSION; MORTALITY; COST; DOCUMENTATION; MORBIDITY; DISORDERS; LENGTH AB The determination of an appropriate level of prospective payment for inpatient medical services requires consideration and documentation of psychiatric problems which impact on resource utilization. A major source of information for reimbursement planning is the list of secondary diagnoses referred to as ''complications and comorbidities'' (CCs) taken from the medical record. If psychiatry problems are omitted on the attestation sheet, they are unlikely to be included in any reimbursement formulae. This study was designed to look at actual hospital experience in terms of how often psychiatric diagnoses were attested to on the medical record. Of the 100 patients evaluated, 25 were found to have 33 psychiatric complications and CCs. Of the 33 psychiatric CCs, only 9 (24%) were recorded on the attestation sheer. Reasons for and implications of this low rare of attestation are discussed. The complete and accurate attestation of psychiatric problems may be the single most important priority for psychiatrists in general hospitals. Even when the DRG system is replaced by capitation payment, the importance of accurate diagnostic recording and recognition will remain paramount to making rate analyses and adjustments. C1 BROWN UNIV,DEPT PSYCHIAT,PROVIDENCE,RI 02912. BROWN UNIV,DEPT MED,PROVIDENCE,RI 02912. WOMEN & INFANTS HOSP RHODE ISL,PROVIDENCE,RI. HARVARD UNIV,MASSACHUSETTS GEN HOSP,BOSTON,MA. MCLEAN HOSP PROGRAM,BOSTON,MA. HEALTHCARE MANAGEMENT ADVISORS INC,ALPHARETTA,GA. RP Goldberg, RJ (reprint author), BROWN UNIV,RHODE ISL HOSP,DEPT PSYCHIAT,PROVIDENCE,RI 02903, USA. NR 25 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD MAR PY 1996 VL 18 IS 2 BP 102 EP 105 DI 10.1016/0163-8343(95)00128-X PG 4 WC Psychiatry SC Psychiatry GA UA263 UT WOS:A1996UA26300003 PM 8833578 ER PT J AU Cleghon, V Gayko, U Copeland, TD Perkins, LA Perrimon, N Morrison, DK AF Cleghon, V Gayko, U Copeland, TD Perkins, LA Perrimon, N Morrison, DK TI Drosophila terminal structure development is regulated by the compensatory activities of positive and negative phosphotyrosine signaling sites on the Torso RTK SO GENES & DEVELOPMENT LA English DT Article DE receptor tyrosine kinase; drosophila; Torso; Corkscrew ID RECEPTOR TYROSINE KINASE; EMBRYONIC TERMINI; GENE TAILLESS; BODY PATTERN; PHOSPHATASE; TRANSDUCTION; ACTIVATION; ENCODES AB Specification of cell fates in the nonsegmented terminal regions of developing Drosophila embryos is under the control of a signal transduction pathway mediated by the receptor tyrosine kinase Torso (Tor). Here, we identify tyrosines (Y) 630 and 918 as the major sites of Tor autophosphorylation. We demonstrate that mutation of Y630, a site required for association with and tyrosine phosphorylation of the tyrosine phosphatase Corkscrew, decreases the efficiency of Tor signaling. In contrast, mutation of Y918, a site capable of binding mammalian rasGAP and PLC-gamma 1, increases Tor signaling. Interestingly, when receptors contain mutations in both the Y630 and Y918 sites, Tor signaling is restored to wild-type levels. These results identify a novel mechanism whereby Tor function is regulated using compensatory signals generated from distinct autophosphorylation sites and reveal an underlying signaling pathway for terminal development. C1 NCI,FREDERICK CANC RES & DEV CTR,ABL BASIC RES PROGRAM,CELLULAR GROWTH MECHANISMS SECT,FREDERICK,MD 21702. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LAB,BOSTON,MA 02114. RI Perrimon, Norbert/F-9766-2011 NR 44 TC 40 Z9 40 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD MAR 1 PY 1996 VL 10 IS 5 BP 566 EP 577 DI 10.1101/gad.10.5.566 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA TZ839 UT WOS:A1996TZ83900005 PM 8598287 ER PT J AU Gudmundsson, A Carnes, M AF Gudmundsson, A Carnes, M TI Geriatric assessment: Making it work in primary care practice SO GERIATRICS LA English DT Article ID CONTROLLED CLINICAL-TRIAL; FUNCTIONAL ASSESSMENT; CONSULTATION TEAM; OLDER PATIENTS; INSTRUMENTS AB Geriatric assessment has become an established part of medical practice, a trend driven by the growing population of older patients, positive patient outcomes, and increased interest in controlling healthcare costs, Geriatric assessments, is a diagnostic process that can be performed in a variety of clinical settings, including the primary care office. The interdisciplinary assessment team usually includes at least three members: a physician, a nurse, and a social worker. Patients who appear to derive the greatest benefit are over age 75, have mild to moderate disabilities, may be at risk of nursing home placement, and may have a poor social network. For optimal effectiveness, assessment must be coupled with a comprehensive therapeutic plan and long-term follow-up. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,MADISON,WI. RP Gudmundsson, A (reprint author), UNIV WISCONSIN,SCH MED,MADISON,WI 53706, USA. NR 25 TC 3 Z9 3 U1 5 U2 7 PU ADVANSTAR COMMUNICATIONS PI DULUTH PA 131 W FIRST ST, DULUTH, MN 55802 SN 0016-867X J9 GERIATRICS JI Geriatrics PD MAR PY 1996 VL 51 IS 3 BP 55 EP & PG 6 WC Geriatrics & Gerontology SC Geriatrics & Gerontology GA UA266 UT WOS:A1996UA26600009 PM 8641592 ER PT J AU Alonso, A Rutan, JS AF Alonso, A Rutan, JS TI Activity/nonactivity and the group therapist: ''Don't just do something, sit there'' SO GROUP LA English DT Article DE abstinent analytic stance; psychodynamic group therapy; psychotherapy; therapist neutrality; therapist nonactivity AB The abstinent stance of psychoanalytically-oriented clinicians is often confused with passivity or coldness toward the patient or the group. Given the current move toward more active, shorter-term treatment, this paper offers a reaffirmation of the value of the abstinent analytic stance. The theoretical rationale for the technique is reviewed, and some specific arguments are made to illustrate the continuing importance of the method in the treatment of patients in psychodynamic group psychotherapy. C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,CTR GRP THERAPY,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR PSYCHOANALYT STUDIES,BOSTON,MA 02114. NR 8 TC 2 Z9 2 U1 0 U2 0 PU HUMAN SCI PRESS INC PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013-1578 SN 0362-4021 J9 GROUP JI Group PD MAR PY 1996 VL 20 IS 1 BP 43 EP 55 DI 10.1007/BF02108604 PG 13 WC Psychology, Clinical SC Psychology GA VT519 UT WOS:A1996VT51900003 ER PT J AU Bauman, NM Eavy, RD Friedman, EM AF Bauman, NM Eavy, RD Friedman, EM TI Infratemporal fossa mass in a pediatric patient SO HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK LA English DT Editorial Material C1 UNIV IOWA HOSP & CLIN,DEPT OTOLARYNGOL HEAD & NECK SURG,IOWA CITY,IA 52242. MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. BAYLOR COLL MED,DEPT OTOLARYNGOL & COMMUN SCI,HOUSTON,TX. OI bauman, nancy/0000-0002-9010-8511 NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1043-3074 J9 HEAD NECK-J SCI SPEC JI Head Neck-J. Sci. Spec. Head Neck PD MAR-APR PY 1996 VL 18 IS 2 BP 188 EP 191 DI 10.1002/1097-0347(199603/04)18:2<188::AID-HED2880180202>3.0.CO;2-# PG 4 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA TX645 UT WOS:A1996TX64500014 PM 8647685 ER EF